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Pancreatic carcinoma is associated with one of the worst clinical outcomes throughout the globe because of its aggressive, metastatic, and drug-resistant nature. During the past decade, several studies have shown that oral, gut, and tumor microbiota play a critical role in the modulation of metabolism and immune responses. Growing pieces of evidence have proved beyond a doubt that the microbiota has a unique ability to influence the tumor microenvironment as well as the metabolism of chemotherapeutic agents or drugs. Given this, microbiota, known as the ecological community of microorganisms, stands to be an avenue of quality research. In this review, we provide detailed and critical information on the role of oral, gut, and pancreatic microbiota disruptions in the development of pancreatic carcinoma. Moreover, we comprehensively discuss the different types of microbiota, their potential role, and mechanism associated with pancreatic carcinoma. The microbiome provides the unique opportunity to enhance the effectiveness of chemotherapeutic agents and immunotherapies for pancreatic cancer by maintaining the right type of microbiota and holds a promising future to enhance the clinical outcomes of patients with pancreatic carcinoma.

Aims: Nonsteroidal anti-inflammatory drugs, including ketoprofen, induce adverse effects within the gastrointestinal (GI)-tract. Hydrogen sulfide (H2S) is an antioxidative gaseous mediator contribu...

Significance: Hydrogen sulfide (H2S), an important regulator of physiology and health, helps resolve inflammation and promotes tissue repair in the gastrointestinal tract. Recent Advances: Gut microbiota live as a multispecies biofilm in close interaction with the upper mucus layer lining the epithelium. The relative abundance, spatial organization, and function of these microorganisms affect a broad range of health outcomes. This article provides a state-of-the-art review of our understanding of the cross talk between H2S, the gut microbiota, and health. H2S can have toxic or therapeutic effects, depending on its concentration and source. When produced at excessive concentrations by local microbiota, H2S may cause mucus disruption and inflammation and contribute to development of cancer. In contrast, low levels of endogenous or exogenous H2S directly stabilize mucus layers, prevent fragmentation and adherence of the microbiota biofilm to the epithelium, inhibit the release of invasive pathobionts, and help resolve inflammation and tissue injury. Although scarce, research findings suggest that dietary H2S obtained from plants or ingestion of the H2S precursor, L-cysteine, may also modulate the abundance and function of microbiota. Critical Issues: A critical issue is the lack of understanding of the metagenomic, transcriptomic, and proteomic alterations that characterize the interactions between H2S and gut microbiota to shape health outcomes. Future Directions: The ambivalent roles of H2S in the gut offer a fertile ground for research on such critical issues. The findings will improve our understanding of how H2S modulates the microbiota to affect body function and will help identify novel therapeutic strategies.

Inflammation is a double-edged sword exhibiting multifaceted functions. On one hand, it either induces tumor cell apoptosis, or establishes tumor dormancy by inhibiting tumor cell proliferation; on the other hand, it either facilitates the tumorigenesis process or reawakens dormant tumor cells, resulting in disease recurrences. Each outcome would depend on the balance between type I and type II inflammation as well as the duration of inflammation being acute or chronic. In this essay, we provide a critical review of the empirical evidence suggesting that chronic inflammation, dominated by type I inflammatory cells and cytokines as a result of trauma and microbiome dysbiosis, could facilitate the carcinogenesis process in normal cells and retain nascent transformed cells in a dormant state. On the other hand, an elevated type II inflammation along with inefficient resolution of type I inflammation following trauma or major surgeries could delay the wound healing process and promote the growth and reawakening of dormant tumor cells, resulting in disease recurrences. Finally, cytokines exhibiting type I and II inflammatory functions, simultaneously, tend to promote tumor recurrence when become chronic. Therefore, the risk of reawakening dormant tumor cells should be considered in cancer survivors who experience major surgeries and trauma, or suffer from chronic inflammatory diseases.

Inflammatory bowel disease is the result of an inappropriate immune response to environmental factors in a genetically susceptible host. The intestinal microbiota has been considered one of the key environmental factors in this disease process, and early influences on the structure of the intestine’s bacterial communities may lead to a dysbiotic state. The complicated relationship between dysbiosis and the developing host immune system, including the innate and adaptive immune systems as well as the intestinal epithelial interface, can have profound effects on the health and disease of the host. Therapies targeted at the gut microbiota continue to be investigated as potential interventions for inflammatory bowel disease.

Collembola are a key component of the soil biota globally, playing an important role in community and ecosystem dynamics. Equally significant are their associated microbiomes, that can contribute to key metabolic functions. In the present study, we investigated the bacterial community composition of four Antarctic springtail species to assess if and how the extreme Antarctic environment has shaped the collembolans’ microbiomes. Springtails were collected from two biogeographical regions, the maritime and the continental Antarctic. From each region, two endemic species, belonging to the genera Cryptopygus (Isotomidae, Entomobryomorpha) and Friesea (Neanuridae, Poduromorpha), were included. This experimental design allowed us to quantify the relative importance of ecological factors (different regions of occurrence) and/or phylogenetic divergence in the host (different Orders) in shaping the Collembola microbiome. The diversity and richness of springtail microbiomes was lower in the Antarctic taxa compared to published information from species from temperate regions. The microbiome composition was predominantly species-specific, with a limited core microbiome shared across the four species examined. While both geographic origin and host species influenced the associated microbiomes, the former was the prevalent driver, with closer similarity between springtails from the same bioregion than between those belonging to the same genus.

The maternal microbiome is understood to be the principal source of the neonatal microbiome but the consequences of intestinal nematodes on pregnant and lactating mothers and implications for the neonatal microbiome are unknown. Using pregnant CD1 mice infected with Heligmosomoides bakeri, we investigated the microbiomes in maternal tissues (intestine, vagina, and milk) and in the neonatal stomach using MiSeq sequencing of bacterial 16S rRNA genes. Our first hypothesis was that maternal nematode infection altered the maternal intestinal, vaginal, and milk microbiomes and associated metabolic pathways. Maternal nematode infection was associated with increased beta-diversity and abundance of fermenting bacteria as well as Lactobacillus in the maternal caecum 2 days after parturition, together with down-regulated carbohydrate, amino acid and vitamin biosynthesis pathways. Maternal nematode infection did not alter the vaginal or milk microbiomes. Our second hypothesis was that maternal infection would shape colonization of the neonatal microbiome. Although the pup stomach microbiome was similar to that of the maternal vaginal microbiome, pups of infected dams had higher beta-diversity at day 2, and a dramatic expansion in the abundance of Lactobacillus between days 2 and 7 compared with pups nursing uninfected dams. Our third hypothesis that maternal nematode infection altered the composition of neonatal microbiomes was confirmed as we observed up-regulation of several putatively beneficial microbial pathways associated with synthesis of essential and branched-chain amino acids, vitamins, and short-chain fatty acids. We believe this is the first study to show that a nematode living in the maternal intestine is associated with altered composition and function of the neonatal microbiome.

Heavy reliance on synthetic pesticides for crop protection has become increasingly unsustainable, calling for robust alternative strategies that do not degrade the environment and vital ecosystem services. There are numerous reports of successful disease control by various microbes used in small-scale trials. However, inconsistent efficacy has hampered their large-scale application. A better understanding of how beneficial microbes interact with plants, other microbes, and the environment and which factors affect disease control efficacy is crucial to deploy microbial agents as effective and reliable pesticide alternatives. Diverse metabolites produced by plants and microbes participate in pathogenesis and defense, regulate the growth and development of themselves and neighboring organisms, help maintain cellular homeostasis under various environmental conditions, and affect the assembly and activity of plant and soil microbiomes. However, research on the metabolites associated with plant health-related processes, except antibiotics, has not received adequate attention. This review highlights several classes of metabolites known or suspected to affect plant health, focusing on those associated with biocontrol and belowground plant–microbe and microbe–microbe interactions. The review also describes how new insights from systematic explorations of the diversity and mechanism of action of bioactive metabolites can be harnessed to develop novel crop protection strategies.

Optimising the production of insects for food and feed and ensuring their health are growing concerns for producers. Insects suffer from a range of insect pathogenic microorganisms, and the management of such diseases is essential. One solution is the introduction of beneficial probiotic bacteria into the diet of the insects. Here, we show that a lactic acid bacterial strain, Pediococcus pentosaceus, isolated from the gut of the mealworm, Tenebrio molitor, was able to inhibit the growth of selected insect pathogens in vitro. Using in vivo assessments of the host’s fitness benefits conferred by the lactic bacterium we show a significant effect of P. pentosaceus on larval growth rate and survival into adulthood. Gut microbiota analysis focusing on bacterial composition based on 16S rRNA gene amplicon sequencing suggests that P. pentosaceus could have successfully colonised the guts, or altered their bacteria, of the larvae that received it. Finally, we discuss our results in the context of mass insect production systems and outline the remaining work needed to explore and secure the role of beneficial bacterial additives in the field.

Antibiotic-associated diarrhea arises when the antibio­tic disrupts the ecology of the intestinal microbiota, by altering the diversity and number of bacteria in the gut. These changes can affect the capacity of the resident microbiota to resist the invasion of pathogenic microorganisms or the overgrowth of opportunistic pathogens species that are endogenously present in the microbiome. Therefore, antibiotic-associated diarrhea may result in prolonged hospitalization, increased health care costs and other complications. Diarrhea is most frequently associated with the use of broad-spectrum antibiotics. Probiotics are “live microorganisms that, when administered in adequate amounts, confer a health be­nefit on the host”. Numerous clinical researches evaluate the efficacy of Lactobacillus rhamnosus GG in the prevention of antibiotic-associated diarrhea. The aim of our research was to study the efficacy of the probiotic Probiolog Baby in children aged from 4 months to 9 years with antibiotic-associated diarrhea, and to investigate its effect on dysbiotic bowel changes. We observed 28 children aged from 4 months to 9 years (average age 4.6 ± 1.9 years) with antibiotic-associated diarrhea, including 57 % of boys and 43 % of girls. The children received the probiotic Probiolog Baby — 1 stick daily for 10 days. In 10 days, only 2 children (7.2 %) had complaints about diarrhea against 100 % at the beginning of our research. The use of Lactobacillus rhamnosus GG (ATCC 53103) in children with antibiotic-associated diarrhea helps reduce diarrhea, colic, bloating, nausea, vomiting, anxiety and poor sleep in children. Considering the combined effect of Lactobacillus rhamnosus GG strain, it can be argued that Probiolog Baby increases the levels of bifidobacteria and lactobacilli in the stool and also reduces the growth of Candida and pathogenic intestinal flora., Антибиотикоассоциированная диарея (ААД) возникает тогда, когда антибиотик нарушает экологию микробиоты кишечника, изменяя разнообразие и количество бактерий в нем. Эти изменения могут повлиять на способность резидентной микробиоты противостоять вторжению патогенных микроорганизмов или росту условно-патогенных видов, которые эндогенно присутствуют в микробиоме. Поэтому AAД может привести к длительной госпитализации, увеличению расходов и ухудшению качества жизни. Диарея чаще всего связана с применением антибиотиков широкого спектра действия. Пробиотики — это «живые микроорганизмы, которые при применении в достаточном количестве приносят пользу здоровью хозяина». Многочисленные клинические исследования изучают эффективность Lactobacillus rhamnosus GG для предотвращения ААД. Целью работы было изучить эффективность применения препарата Пробиолог Бейби у детей в возрасте от 4 мес. до 9 лет жизни с диагнозом антибиотикоассоциированной диареи, а также исследовать его влияние на дисбиотические изменения кишечника. Под нашим наблюдением находилось 28 детей в возрасте от 4 мес. до 9 лет (средний возраст — 4,6 ± 1,9 года) с диагнозом антибиотикоассоциированной диареи, среди них 57 % мальчиков и 43 % девочек. Дети получали Пробиолог Бейби по 1 стику в день в течение 10 дней. Через 10 дней только у 2 детей (7,2 %) были жалобы на диарею против 100 % в начале наблюдения. Применение штамма Lactobacillus rhamnosus GG (АТСС 53103) у детей с антибиотикоассоциированной диареей способствует уменьшению диареи, колик, вздутия живота, тошноты, рвоты, беспокойства и плохого сна. Принимая во внимание комплексное воздействие штамма Lactobacillus rhamnosus GG, можно утверждать, что Пробиолог Бейби увеличивает уровень бифидобактерий и лактобактерий в кале, а также уменьшает рост грибов рода Candida и патогенной кишечной флоры., Антибіотикоасоційована діарея (ААД) виникає тоді, коли антибіотик порушує екологію мікробіоти кишечника, змінюючи різноманітність і кількість бактерій у ньому. Ці зміни можуть вплинути на здатність резидентної мікробіоти протистояти вторгненню патогенних мікроорганізмів або зростанню умовно-патогенних видів, що ендогенно присутні в мікробіомі. Тому AAД може призвести до тривалої госпіталізації, збільшення витрат і погіршення якості життя. Діарея найчастіше пов’язана із застосуванням антибіотиків широкого спектра дії. Пробіотики — це «живі мікроорганізми, які при застосуванні в достатній кількості дають користь здоров’ю хазяїна». Численні клінічні дослідження вивчають ефективність Lactobacillus rhamnosus GG для запобігання ААД. Метою роботи було вивчити ефективність застосування препарату Пробіолог Бейбі у дітей віком від 4 міс. до 9 років життя з діагнозом антибіотикоасоційованої діареї, а також дослідити його вплив на дисбіотичні зміни кишок. Під нашим спостереженням перебували 28 дітей віком від 4 міс. до 9 років (середній вік 4,6 ± 1,9 року) з діагнозом антибіотикоасоційованої діареї, серед них 57 % хлопчиків і 43 % дівчаток. Діти отримували Пробіолог Бейбі по 1 стіку на день протягом 10 днів. Через 10 днів лише у 2 дітей (7,2 %) були скарги на діарею проти 100 % на початку спостереження. Застосування штаму Lactobacillus rhamnosus GG (АТСС 53103) у дітей з антибіотикоасоційованою діареєю сприяє зменшенню діареї, кольок, здуття живота, нудоти, блювання, неспокою і поганого сну. Беручи до уваги комплексний вплив штаму Lactobacillus rhamnosus GG, можна стверджувати, що Пробіолог Бейбі збільшує рівень біфідобактерій і лактобактерій у випорожненнях, а також зменшує ріст грибків роду Candida й патогенної кишкової флори.

Fecal microbiota transplantation (FMT) is a highly effective therapeutic procedure for treating recurrent Clostridium difficile infection. However, the effectiveness of the FMT for the treatment of other chronic diseases associated with intestinal dysbiosis, until recently, remained very low and very variable. A number of studies conducted in recent years have suggested that the success of the FMT is largely dependent on the microbial diversity and composition of the donor stool, which has led to the concept of the existence of FMT superdonors, which are considered individuals whose FMT is accompanied by a high efficiency. The review presents some of the results of the FMT with the involvement of superdonors, describes the possible mechanisms and factors affecting the success of the FMT. It is concluded that the high diversity of the gut microbiota, especially in the donor, seems to be the best predictor of the patient’s response to the FMT. It is assumed that the identification and subsequent characterization of superdonor intestinal microbiomes will improve our understanding of the microbial component of chronic diseases and will allow the use of the FMT in a more targeted manner in the future.

Background. The microbiome of the pre-epithelial biofilm of the large intestine in direct contact with the body also interacts with the immune and other systems that emphasizes the urgency of its study in various diseases. The purpose of the study was to determine the taxonomic composition, population level, analytical microecological indicators and the degree of microecological disorders of the pre-epithelial biofilm of the large intestine in albino rats with thyrotoxicosis. Materials and methods. Experiments were carried out on 25 mature male albino rats weighing 220–240 g, of which 15 animals were included to the control group (intact animals), and 10 rats — to the main group. The experimental thyrotoxicosis was simulated by intragastric administration of L-thyroxine for 14 days. Under sterile conditions, a laparotomy was performed, a segment (up to 3 cm) of the large intestine with its contents was taken. The washed portion of the intestine was homogenized with a sterile 0.9% NaCl solution. A series of ten-fold dilutions with 10 –2 to 10 –7 concentrations of the initial mixture were prepared. From each tube, 0.01 ml were seeded on solid optimal nutrient media with subsequent isolation and identification of microbes according to morphological, tinctorial, cultural and biochemical properties. Results. In some animals, bifidobacteria and lactobacilli, as well as bacteroides and escherichia, are eliminated. A significant deficiency of not only bifidobacteria by 48.50 % and lactobacillus by 94.59 %, but also of bacteroides by 44.85 % was established. Determination of the quantitative dominance of each taxon showed that the dominant role of bifidobacteria in the microbiocenosis is reduced by 82.76 %, lactobacillus — by 2.20 times, and the role of bacteroides in the microbiocenosis of the epithelial biofilm of the large intestine of albino rats with the experimental thyrotoxicosis — by 43.04 %, E.coli — by 7.18 %, but the role of opportunistic enterobacteria and staphylococci, which contaminated and colonized the mucosa of the large intestine, increased substantially. Conclusions. Experimental thyrotoxicosis is accompanied by a partial elimination from the biotope of the pre-epithelial biofilm of the large intestine of bifidobacteria and lactobacilli, as well as bacteroides. There comes elimination from the colic mucous membrane in all experimental animals of peptostreptococcus, clostridia and enterococci, as well as colonization of the biotope with opportunistic enterobacteria (proteus, klebsiella) and staphylococci.

Airway dysbiosis has been associated with lung disease severity in patients with cystic fibrosis (CF). However, the relationship between dysbiosis, airway inflammation and lung function impairement remains poorly understood. The aim of this study was therefore to determine how the structure of the sputum microbiota, airway inflammation markers and spirometry are related in patients with CF. Sputum samples were collected from 106 CF patients between 12 and 72 years. These were analyzed by 16S rRNA gene amplicon sequencing. Moreover, levels of pro-inflammatory cytokines (IL-1β, IL-8, IL-6 and TNF-α) and Neutrophil elastase (NE) were determined. The relationship between the microbiota, inflammation markers and forced expiratory volume in one second percent predicted (FEV1% predicted) was evaluated by multi-parameter analysis. The microbiota α-diversity correlated inverse with inflammation markers IL-1β, IL-8, TNF-α, NE and positively with FEV1% predicted. Patients could be divided into 7 clusters based on their microbiota structure. The most diverse cluster was defined by oropharyngeal-like flora (OF) while the others were characterized by the dominance of a single pathogen. Patients with the diverse OF microbiota cluster had lower sputum inflammatory markers and higher FEV1% predicted compared to patients with a pathogen-dominated microbiota including Pseudomonas aeruginosa. Our results suggest that the diversity of the airway microbiota is an important biomarker of the severity of airway inflammation linking dysbiosis to lung function decline in patients with CF.

Recent evidence supports a role for the gut microbiota in hypertension, but whether ambulatory blood pressure is associated with gut microbiota and their metabolites remains unclear. We characterized the function of the gut microbiota, their metabolites and receptors in untreated human hypertensive participants in Australian metropolitan and regional areas. Ambulatory blood pressure, fecal microbiome predicted from 16S rRNA gene sequencing, plasma and fecal metabolites called short-chain fatty acid, and expression of their receptors were analyzed in 70 untreated and otherwise healthy participants from metropolitan and regional communities. Most normotensives were female (66%) compared with hypertensives (35%, P Acidaminococcus spp ., Eubacterium fissicatena, and Muribaculaceae were higher, while Ruminococcus and Eubacterium eligens were lower in hypertensives. Importantly, normotensive and essential hypertensive cohorts could be differentiated based on gut microbiome gene pathways and metabolites. Specifically, hypertensive participants exhibited higher plasma acetate and butyrate, but their immune cells expressed reduced levels of short-chain fatty acid-activated GPR43 (G-protein coupled receptor 43). In conclusion, gut microbial diversity did not change in essential hypertension, but we observed a significant shift in microbial gene pathways. Hypertensive subjects had lower levels of GPR43, putatively blunting their response to blood pressure-lowering metabolites.

Resumen: Introducción: El papel de la microbiota en los modelos animales de esclerosis múltiple está bien establecido; por el contrario, los estudios en humanos son escasos. Métodos: Estudio transversal descriptivo que compara la composición relativa de la microbiota intestinal en 30 pacientes con esclerosis múltiple (15 tratados con interferón β-1b, 15 sin tratamiento) y 14 controles sanos utilizando la secuenciación de última generación. Resultados: Los sujetos control y los pacientes con esclerosis múltiple presentaron diferente abundancia de los filos Euryarchaeota, Firmicutes, Proteobacteria, Actinobacteria, y Lentisphaerae y 17 especies bacterianas. Concretamente, la abundancia en Firmicutes, Actinobacteria y Lentisphaerae y 6 especies mostró diferencias al comparar los grupos control y sin tratamiento, desapareciendo esta diferencia cuando se compararon con los pacientes tratados. Se observó reducción estadísticamente significativa en la abundancia de Prevotella copri en pacientes sin tratamiento en comparación con controles, mientras que los tratados con interferón β-1b presentaron un aumento significativo frente a pacientes sin tratamiento, asemejándose al grupo de pacientes sanos control. Conclusión: La composición de la microbiota intestinal fue diferente entre los pacientes con esclerosis múltiple y los controles, y entre los pacientes sin tratamiento y los tratados con interferón β-1b. En la mayoría de los casos, no se encontraron diferencias entre los pacientes tratados y los controles sanos, siendo especialmente evidente con P. copri. Esto podría indicar que la influencia del interferón β-1b sobre la microbiota intestinal podría subyacer en los beneficios clínicos observados en pacientes con esclerosis múltiple que siguen este tratamiento. Serán necesarios estudios longitudinales y funcionales para poder mostrar causalidad. Abstract: Introduction: The association between gut microbiota and animal models of multiple sclerosis has been well established; however, studies in humans are scarce. Methods: We performed a descriptive, cross-sectional study comparing the relative composition of gut microbiota in 30 patients with multiple sclerosis (15 treated with interferon β–1b, 15 not receiving this treatment) and 14 healthy controls using next generation sequencing. Results: Patients with multiple sclerosis and controls showed differences in the proportion of Euryarchaeota, Firmicutes, Proteobacteria, Actinobacteria, and Lentisphaerae phyla and in 17 bacterial species. More specifically, we found significant differences in the proportion of Firmicutes, Actinobacteria, and Lentisphaerae and 6 bacteria species between controls and untreated patients; however, these differences disappeared when compared with treated patients. Untreated patients showed a significant reduction in the proportion of Prevotella copri compared to controls, while the bacteria was significantly more abundant in patients treated with interferon β–1b than in untreated patients, with levels resembling those observed in the healthy control group. Conclusion: We observed differences in gut microbiota composition between patients with multiple sclerosis and controls, and between patients treated and not treated with interferon β–1b. In most cases, no differences were observed between treated patients and healthy controls, particularly for P. copri levels. This suggests that the clinical improvements observed in patients with multiple sclerosis receiving interferon β–1b may result from the effect of the drug on gut microbiota. Longitudinal and functional studies are necessary to establish a causal relationship.

Objectives The hospital environment has been implicated in the enrichment and exchange of pathogens and antibiotic resistance, but its potential in shaping the symbiotic microbial community of hospital staff is unclear. This study was designed to evaluate the alteration of the gut microbiome in medical workers compared to non-medical controls. Methods A prospective cross-sectional cohort study was conducted in the intensive care unit (ICU) and other departments of a centre in north-eastern China. Faecal samples of 175 healthy medical workers—short-term (1–3 months) workers (n = 80) and long-term (>1 year) workers (n = 95)—and 80 healthy non-medical controls were analysed using 16S rRNA amplicon sequencing. The hospital environmental samples (n = 9) were also analysed. Results The gut microbiomes of medical workers exhibited marked deviations in diversity and alteration in microbial composition and function. Short-term workers showed significantly higher abundances of taxa such as Lactobacillus, Butyrivibrio, Clostridiaceae, Clostridium, Ruminococcus, Dialister, Bifidobacterium, Odoribacter, and Desulfovibrio and lower abundances of Bacteroides and Blautia than the controls. Long-term workers showed higher abundances of taxa such as Dialister, Veillonella, Clostridiaceae, Clostridium, Bilophila, Desulfovibrio, Pseudomonas, and Akkermansia and lower abundances of Bacteroides and Coprococcus than the controls. The medical workers' department (ICU versus non-ICU) and position (resident doctor versus nursing staff) also impacted their gut microbiome. Compared with the non-ICU workers, workers in the ICU showed a significant increase in the abundances of Dialister, Enterobacteriaceae, Phascolarctobacterium, Pseudomonas, Veillonella, and Streptococcus and a marked depletion of Faecalibacterium, Blautia, and Coprococcus. In contrast with the nursing staff, the resident doctors showed a significant increase in Erysipelotrichaceae and Clostridium and a decrease in Bacteroides, Blautia, and Ruminococcus in the gut microbiome. Moreover, we found that the microbiota of hospital environments potentially correlated with the workers' gut microbiota. Conclusions Our findings demonstrated structural changes in the gut microbial community of medical workers.

BACKGROUND: Gastrointestinal dysfunction is a frequent and disabling manifestation of autoimmune polyendocrine syndrome type 1 (APS-1), a rare monogenic multi-organ autoimmune disease caused by the loss of central AIRE-controlled immune tolerance. OBJECTIVE: We aimed to understand the role of the gut microbiome in APS-1 symptoms and potentially alleviate common gastrointestinal symptoms by probiotic intervention. METHODS: We characterized the fecal microbiomes of 28 APS-1 patients and searched for associations with gastrointestinal symptoms, circulating anti-cytokine autoantibodies and tryptophan-related metabolites. We additionally administered daily doses of the probiotic Lactobacillus rhamnosus GG for three months. RESULTS: Of 581 metagenomic operational taxonomic units (mOTUs) characterized in total, 14 were significantly associated with APS-1 compared to healthy controls, with six mOTUs depleted and eight enriched in APS-1 patients. Four overabundant mOTUs were significantly associated with severity of constipation. We observed phylogenetically conserved microbial associations with autoantibodies against cytokines. After the three-month intervention with the probiotic L. rhamnosus GG, a subset of gastrointestinal symptoms were alleviated. L. rhamnosus GG abundance was increased post-intervention and corresponded with decreased abundances of Alistipes onderdonkii and Collinsella aerofaciens, two species positively associated with severity of diarrhea in APS-1 patients. CONCLUSION: The APS-1 microbiome correlates with several APS-1 symptoms, some of which are alleviated after a three-month L. rhamnosus GG intervention. Autoantibodies against cytokines appear to shape the gut microbiome by positively correlating with a taxonomically consistent group of bacteria. CLINICAL IMPLICATIONS: Administration of L. rhamnosus GG appears to alleviate certain gastrointestinal symptoms of APS-1.

Ultra-processed foods are industrially manufactured ready-to-eat or ready-to-heat formulations containing food additives and little or no whole foods, in contrast to processed foods, which are whole foods preserved by traditional techniques such as canning or pickling. Recent epidemiological studies suggest that higher consumption of ultra-processed food is associated with increased risk of cardiovascular disease (CVD). However, epidemiological evidence needs to be corroborated with criteria of biological plausibility. This review summarizes the current evidence on the putative biological mechanisms underlying the associations between ultra-processed foods and CVD. Research ranging from laboratory-based to prospective epidemiological studies and experimental evidence suggest that ultra-processed foods may affect cardiometabolic health through a myriad of mechanisms, beyond the traditionally recognized individual nutrients. Processing induces significant changes to the food matrix, for which ultra-processed foods may affect health outcomes differently than unrefined whole foods with similar nutritional composition. Notably, the highly degraded physical structure of ultra-processed foods may affect cardiometabolic health by influencing absorption kinetics, satiety, glycemic response, and the gut microbiota composition and function. Food additives and neo-formed contaminants produced during processing may also play a role in CVD risk. Key biological pathways include altered serum lipid concentrations, modified gut microbiota and host–microbiota interactions, obesity, inflammation, oxidative stress, dysglycemia, insulin resistance, and hypertension. Further research is warranted to clarify the proportional harm associated with the nutritional composition, food additives, physical structure, and other attributes of ultra-processed foods. Understanding how ultra-processing changes whole foods and through which pathways these foods affect health is a prerequisite for eliminating harmful processing techniques and ingredients.

BACKGROUND: Healthy plant-based diet index (hPDI) is associated with a lower risk of cardiometabolic conditions, but its association as well as interactions with microbiome have not been elucidated. OBJECTIVES: We aimed to investigate the interrelations between hPDI, gut microbiome, and cardiometabolic risk markers. METHODS: hPDI was derived from dietary assessments by a validated FFQ and was examined in relation to metagenomic profiles of 911 fecal samples collected from 303 men aged 71 ± 4 y with an average BMI (in kg/m(2)) of 25.2 ± 3.6 in the Men's Lifestyle Validation Study. Principal coordinate (PCo) analysis based on Bray–Curtis dissimilarity was conducted, and interactions between hPDI and PCo were examined by using a metabolic risk score composed of blood lipids, BMI, and glycated hemoglobin. RESULTS: After multivariable adjustment, hPDI was significantly associated with the relative abundance of 7 species and 9 pathways. In particular, higher hPDI was significantly associated with a higher relative abundance of Bacteroides cellulosilyticus and Eubacterium eligens, amino acid biosynthesis pathways (l-isoleucine biosynthesis I and III and l-valine biosynthesis), and the pathway of pyruvate fermentation to isobutanol. A favorable association between hPDI and the metabolic risk score was more pronounced among men with a higher PCo characterized by higher abundance of Bacteroides uniformis and lower abundance of Prevotella copri. At the individual species level, a similar interaction was also observed between hPDI and P. copri, as well as with Clostridium clostridioforme or Blautia hydrogenotrophica (all P-interaction

Although intestinal microbial communities from anadromous Arctic char (Salvelinus alpinus (Linnaeus, 1758)) in Kitikmeot, Nunavut, Canada, differ depending on the timing and location of capture, determinants of gut microbiota in other wild Arctic salmonids are largely unknown. Using high-throughput 16S rRNA gene sequence data, we compared intestinal microbiota from Arctic char to those from a related and sympatric salmonid, lake whitefish (Coregonus clupeaformis (Mitchill, 1818)). Shifts in lake whitefish gut microbial community composition were observed between brackish water and freshwater, similar to impacts of salinity reported previously for Arctic char. Despite these similarities, gut community profiles for the two salmonids differed, with whitefish having higher diversities and increased proportions of taxa affiliated with potential pathogens. Geography seemed to have a greater impact on freshwater whitefish gut microbiota than on corresponding Arctic char. Additionally, microbiota diversity was significantly more affected by feeding behavior in whitefish compared with sympatric Arctic char. As sampled whitefish were at their northern range limits and grew slowly, we speculate that they, and their microbial consortia, could be more vulnerable to certain abiotic and biotic factors than Arctic char, which are well adapted to conditions found in these high latitude environments and have the most northern distribution of any freshwater fish.

Diet is a key modulator of fecal microbiota composition and function. However, the influence of diet on the microbiota from toddlerhood to adolescence and young adulthood is less well studied than for infancy and adulthood. We aimed to complete a qualitative systematic review of the impacts of diet on the fecal microbiota of healthy humans 1–20 y of age. English-language articles, published after 2008, indexed in the PubMed/MEDLINE, Cochrane, Web of Science, and Scopus databases were searched using keywords and Medical Subject Headings terms. Quality assessment of included studies was conducted using the Quality Criteria Checklist derived from the Nutrition Evidence Library of the Academy of Nutrition and Dietetics. A total of 973 articles were identified through database searching and 3 additional articles were included via cross-reference. Subsequent to de-duplication, 723 articles were screened by title and abstract, of which 709 were excluded based on inclusion criteria established a priori. The remaining 14 studies were independently screened by 2 reviewers for final inclusion. Included studies were published between 2010 and 2019 and included 8 comparative cross-sectional studies, 4 cross-sectional studies, 1 randomized crossover study, and 1 substudy of a randomized 2-period crossover trial. Associations of a diet rich in indigestible plant polysaccharides with Prevotella, or with an enterotype dominated by this genus, often comprised of the species Prevotella copri, were observed. In addition, associations of a high-fat and -sugar diet with Bacteroides, or with an enterotype dominated by this genus, were observed predominantly in comparative cross-sectional and cross-sectional studies spanning the ages of 1–15 y. This review identified a gap in the literature for ages 16–20 y. In addition, randomized controlled trials for dietary intervention are needed to move from association-based observations to causal relations between diet and microbiota composition and function. This systematic review was registered at www.crd.york.ac.uk/prospero as CRD42020129824.

The microbiota plays essential roles in health and disease, in both the intestine and the extra-intestine. Dysbiosis of the gut microbiota causes dysfunction in the intestine, which leads to inflammatory, immune, and infectious diseases. Dysbiosis is also associated with diseases beyond the intestine via microbial translocation or metabolisms. The in situ breast microbiome, which may be sourced from the gut through lactation and sexual contact, could be altered and cause breast diseases. In this review, we summarize the recent progress in understanding the interactions among the gut microbiome, breast microbiome, and breast diseases. We discuss the intestinal microbiota, microbial metabolites, and roles of microbiota in immune system. We emphasize the novel roles and mechanisms of the microbiome (both in situ and gastrointestinal sourced) and bacterial products in the development and progression of breast cancer. The intestinal microbial translocation suggests that the gut microbiome is translocated to the skin and subsequently to the breast tissue. The gut bacterial translocation is also due to the increased intestinal permeability. The breast and intestinal microbiota are important factors in maintaining healthy breasts. Micronutrition queuine (Q) is derived from a de novo synthesized metabolite in bacteria. All human cells use queuine and incorporate it into the wobble anticodon position of specific transfer RNAs. We have demonstrated that Q modification regulates genes critical in tight junctions and migration in human breast cancer cells and a breast tumor model. We further discuss the challenges and future perspectives that can move the field forward for prevention, diagnosis, and treatment of breast diseases.

Chilhuacle negro chili (Capsicum annuum L.) is an ancient Mexican landrace that is deeply linked to the culinary heritage of the country. Because of the high profitability and uniqueness of this crop, the Universidad Autónoma del Estado de Morelos is exploring its production in controlled environments. In the crop cycles of 2018 to 2019, the production of chilhuacle negro plants was seriously affected by an unidentified pathogen causing fruit rot, which reduced its quality, yield, and market value. Therefore, the main objective of this work was to study and characterize the fruit microbiota, which could help reveal the causal agent of this disease. Using DNA metabarcoding coupled with Illumina and nanopore sequencing technologies, we collected and analyzed both healthy and infected chili fruit, along with greenhouse bioaerosols. We also explored the bacterial and fungal microbiota by using microbiological techniques to isolate some of the culturable bacterial and fungal species. Our results suggest that the seedborne fungus Alternaria alternata is activated during the maturation stage of chilhuacle negro fruit, triggering a microbiome imbalance, which may in turn enable the establishment of other opportunistic pathogenic fungi during fruit decay, such as Mucor sp. To our knowledge, this is the first study of the chilhuacle negro chili microbiome, which can shed some light on our understanding of one of the main diseases that affect this valuable crop.

Despite the impact of childhood diarrhea on morbidity and mortality, our understanding of its sequelae has been significantly hampered by the lack of studies that examine samples across the entire intestinal tract. Infant rhesus macaques are naturally susceptible to human enteric pathogens and recapitulate the hallmarks of diarrheal disease such as intestinal inflammation and growth faltering. Here, we examined intestinal biopsies, lamina propria leukocytes, luminal contents, and fecal samples from healthy infants and those experiencing growth faltering with distant acute or chronic active diarrhea. We show that growth faltering in the presence or absence of active diarrhea is associated with a heightened systemic and mucosal pro-inflammatory state centered in the colon. Moreover, polyclonal stimulation of colonic lamina propria leukocytes resulted in a dampened cytokine response, indicative of immune exhaustion. We also detected a functional and taxonomic shift in the luminal microbiome across multiple gut sites including the migration of Streptococcus and Prevotella species between the small and large intestine, suggesting a decompartmentalization of gut microbial communities. Our studies provide valuable insight into the outcomes of diarrheal diseases and growth faltering not attainable in humans and lays the groundwork to test interventions in a controlled and reproducible setting.

Background: Probiotics can improve immune function leading to the prevention and management of viral infections like SARS-CoV-2 infection (COVID-19 disease). Methods: We searched PubMed, EMBASE, Google Scholar, Science Direct, Scopus, and Web of Science up to May 2020 to identify interventional & observational studies documenting the effects of probiotics on incidence, severity, duration, and other clinical manifestations of viral infections, especially SARS-CoV-2-induced. Results: From a total of 91 records, 24 studies were obtained and classified into three domains based on the efficacy of probiotics on 1) shortening the period and severity of infections (n=9), 2) incidence (n=6), and 3) other clinical complications that may be followed by viral disorders (n=9). Identified probiotics have positive effects on the mentioned domains. Conclusion: Based on the evidence, some probiotic strains may be useful in SARS-CoV-2 infection; randomized trials are needed to show the facts.

Objectives Chronic widespread musculoskeletal pain (CWP) is a characteristic symptom of fibromyalgia, which has been shown to be associated with an altered gut microbiome. Microbiome studies to date have not examined the milder CWP phenotype specifically nor have they explored the role of raised BMI. The aim of this study was to investigate whether the microbiome is abnormal in CWP. Methods CWP was assessed using a standardized screening questionnaire in female volunteers from the TwinsUK cohort including 113 CWP cases and 1623 controls. The stool microbiome was characterized using 16S rRNA amplicon sequencing and amplicon sequence variants, and associations with CWP examined using linear mixed-effects models adjusting for BMI, age, diet, family relatedness and technical factors. Results Alpha diversity was significantly lower in CWP cases than controls (Mann–Whitney test, P-values 2.3e-04 and 1.2e-02, for Shannon and Simpson indices respectively). The species Coprococcus comes was significantly depleted in CWP cases (Padj = 3.04e-03). A genome-wide association study (GWAS) performed for C. comes in TwinsUK followed by meta-analysis with three Dutch cohorts (total n = 3521) resulted in nine suggestive regions, with the most convincing on chromosome 4 near the TRAM1L1 gene (rs76957229, P = 7.4e-8). A Mendelian randomization study based on the results of the GWAS did not support a causal role for C. comes on the development of CWP. Conclusions We have demonstrated reduced diversity in the microbiome in CWP, indicating an involvement of the gut microbiota in CWP; prospectively the microbiome may offer therapeutic opportunities for this condition.

OBJECTIVE Systemic inflammatory factors have been implicated in symptomatic hand osteoarthritis (OA). Gut microbiome dysbiosis promotes systemic inflammation. The aim of this study was to examine the association between the gut microbiome and the presence of symptomatic hand OA in a population-based study. METHODS Study participants were subjects of the Xiangya Osteoarthritis Study, a community-based observational study conducted in the Hunan Province of China. Symptomatic hand OA was defined as the presence of both symptoms and radiographic OA in the same hand. The gut microbiome was analyzed using 16S ribosomal RNA gene sequencing in stool samples. We examined the relation of α-diversity, β-diversity, relative abundance of taxa, and potential bacterial functional pathways to symptomatic hand OA. RESULTS A total of 1,388 participants (mean age 61.3 years, 57.4% women) were included in the study, of whom 72 had symptomatic hand OA (prevalence of symptomatic hand OA 5.2%). Beta-diversity of the gut microbiome, but not α-diversity, was significantly associated with the presence of symptomatic hand OA (P = 0.003). Higher relative abundance of the genera Bilophila and Desulfovibrio as well as lower relative abundance of the genus Roseburia was associated with symptomatic hand OA. Most functional pathways (i.e., those annotated in the KEGG Ortholog hierarchy) that were observed to be altered in participants with symptomatic hand OA belonged to the amino acid, carbohydrate, and lipid metabolic pathways. CONCLUSION This large, population-based study provides the first evidence that alterations in the composition of the gut microbiome were observed among study participants who had symptomatic hand OA, and a low relative abundance of Roseburia but high relative abundance of Bilophila and Desulfovibrio at the genus level were associated with prevalent symptomatic hand OA. These findings may help investigators understand the role of the microbiome in the development of symptomatic hand OA and could contribute to potential translational opportunities.

Culture-independent study of the lower respiratory tract after lung transplantation has enabled an understanding of the microbiome – that is, the collection of bacteria, fungi, and viruses, and their respective gene complement – in this niche. The lung has unique features as a microbial environment, with balanced entry from the upper respiratory tract, clearance, and local replication. There are many pressures impacting the microbiome after transplantation, including donor allograft factors, recipient host factors such as underlying disease and ongoing exposure to the microbe-rich upper respiratory tract, and transplantation-related immunosuppression, antimicrobials, and post-surgical changes. To date, we understand that the lung microbiome after transplant is dysbiotic; that is, it has higher biomass and altered composition compared to a healthy lung. Emerging data suggest that specific microbiome features may be linked to host responses, both immune and non-immune, and clinical outcomes such as chronic lung allograft dysfunction (CLAD), but many questions remain. The goal of this review is to put into context our burgeoning understanding of the lung microbiome in the post-lung transplant patient, the interactions between microbiome and host, the role the microbiome may play in post-transplant complications, and critical outstanding research questions.

The equilibrium between host animals and their microbiota has been convincingly linked with overall host health. Numerous reports describe beneficial effects of probiotic microbiota on the health of humans and other species extending to improved immune functions, wound repair capacity, metabolism, and psychiatry. Among candidate unifying host effector molecules is oxytocin, a neuropeptide hormone related to sociability and a sense of physical and mental well-being. It has been shown in mouse models that endogenous oxytocin levels are upregulated after consuming the probiotic Lactobacillus reuteri derived from human breast milk, with interesting evolutionary implications. Using heirloom microbiota such as L. reuteri to naturally upregulate host endogenous oxytocin levels potentially overcomes the known therapeutic challenges of oxytocin's short half-life and obscure brain targets.

Background Diet, the gut microbiota, and microRNAs (miRNAs) have been recognized as factors possibly influencing the pathogenesis of Alzheimer's disease. However, the combined role of diet, the gut microbiota, and miRNAs in mild cognitive impairment (MCI) has not been extensively investigated. Objectives To examine the associations among diet quality, the gut microbiota, miRNAs, and risks of MCI in middle-aged and elderly Chinese population. Methods Participants were drawn from the Effects and Mechanism Investigation of Cholesterol and Oxysterol on Alzheimer's disease (EMCOA) study. We included 2239 participants who completed comprehensive cognitive tests and dietary surveys at baseline and follow-up. Chinese Dietary Guidelines Index 2018 (CDGI-2018), Energy-Adjusted Dietary Inflammatory Index (E-DII) and Healthy Lifestyle Score (HLS) values were calculated based on data from a standard questionnaire. Changes of gut microbiota and serum miRNA expression were detected in 75 MCI and 52 healthy participants. The receiver operating characteristic curve was performed based on a logistic regression model distinguishing patients with MCI from healthy controls. Results Higher CDGI-2018 (RR, 0.75; 95% CI: 0.58-0.98) and HLS (RR, 0.54; 95% CI: 0.34-0.84) values and lower E-DII (RR, 1.46; 95% CI: 1.14-1.87) values were significantly associated with a lower risk of MCI. Lower microbial diversity and abundance of Faecalibacterium, unidentified Ruminococcaceae, and Alistipes were found in MCI participants compared with healthy controls. The abundance of ProteobacteriaandGammaproteobacteria was higher in MCI participants and was correlated with hsa-let-7g-5p, hsa-miR-107, and hsa-miR-186-3p. The predictive signatures of diet quality scores, differential gut microbiota, and serum miRNAs had good performance on distinguishing MCI participants from healthy individuals (AUC = 0.91). Conclusions A better diet quality is associated with a lower risk of MCI, which may be mediated by the microbiota composition and miRNA expression. These findings suggest that diet, the gut microbiota, and miRNAs may serve as a combinatorial biomarker to identify MCI patients and provide new insight for the diagnosis and prevention of MCI. This study was registered at the Chinese Clinical Trial Registry as ChiCTROOC-17011882.

Advances in -omics analyses have tremendously enhanced our understanding of the role of the microbiome in human health and disease. Most research is focused on the bacteriome, but scientists have now realized the significance of the virome and microbial dysbiosis as well, particularly in noninfectious diseases such as cancer. In this review, we summarize the role of mycobiome in tumorigenesis, with a dismal prognosis, and attention to pancreatic ductal adenocarcinoma (PDAC). We also discuss bacterial and mycobial interactions to the host’s immune response that is prevalently responsible for resistance to cancer therapy, including immunotherapy. We reported that the Malassezia species associated with scalp and skin infections, colonize in human PDAC tumors and accelerate tumorigenesis via activating the C3 complement-mannose-binding lectin (MBL) pathway. PDAC tumors thrive in an immunosuppressive microenvironment with desmoplastic stroma and a dysbiotic microbiome. Host-microbiome interactions in the tumor milieu pose a significant threat in driving the indolent immune behavior of the tumor. Microbial intervention in multimodal cancer therapy is a promising novel approach to modify an immunotolerant (“cold”) tumor microenvironment to an immunocompetent (“hot”) milieu that is effective in eliminating tumorigenesis.

Microbiomes not only exist across many different body sites in human beings but also interact dynamically with the host and environment. The unique feature and complexity of 16S ribosomal RNA gene sequence data, especially the sparsity of the data, present challenges to statistical analysis and interpretation. Proper normalization is critical in ensuring the validity of downstream analysis. Modeling the inflated zeros is an active area of research, and it has been extended from differential abundance analysis to a variety of other types of analyses. One specific method may not work well under all conditions, where sample size, effect size, data distribution, and degree of zero inflation vary greatly.

Author(s): Koponen, Kari K; Salosensaari, Aaro; Ruuskanen, Matti O; Havulinna, Aki S; Mannisto, Satu; Jousilahti, Pekka; Palmu, Joonatan; Salido, Rodolfo; Sanders, Karenina; Brennan, Caitriona; Humphrey, Gregory C; Sanders, Jon G; Meric, Guillaume; Cheng, Susan; Inouye, Michael; Jain, Mohit; Niiranen, Teemu J; Valsta, Liisa M; Knight, Rob; Salomaa, Veikko V | Abstract: BackgroundDiet has a major influence on the human gut microbiota, which has been linked to health and disease. However, epidemiological studies on associations of a healthy diet with the microbiota utilizing a whole-diet approach are still scant.ObjectivesTo assess associations between healthy food choices and human gut microbiota composition, and to determine the strength of association with functional potential.MethodsThis population-based study sample consisted of 4930 participants (ages 25-74; 53% women) in the FINRISK 2002 study. Intakes of recommended foods were assessed using a food propensity questionnaire, and responses were transformed into healthy food choices (HFC) scores. Microbial diversity (alpha diversity) and compositional differences (beta diversity) and their associations with the HFC score and its components were assessed using linear regression. Multiple permutational multivariate ANOVAs were run from whole-metagenome shallow shotgun-sequenced samples. Associations between specific taxa and HFC were analyzed using linear regression. Functional associations were derived from Kyoto Encyclopedia of Genes and Genomes orthologies with linear regression models.ResultsBoth microbial alpha diversity (β/SD, 0.044; SE, 6.18n×n10-5; Pn=n2.21n×n10-3) and beta diversity (R2, 0.12; Pn≤n1.00n×n10-3) were associated with the HFC score. For alpha diversity, the strongest associations were observed for fiber-rich breads, poultry, fruits, and low-fat cheeses (all positive). For beta diversity, the most prominent associations were observed for vegetables, followed by berries and fruits. Genera with fiber-degrading and SCFA-producing capacities were positively associated with the HFC score. The HFC score was associated positively with functions such as SCFA metabolism and synthesis, and inversely with functions such as fatty acid biosynthesis and the sulfur relay system.ConclusionsOur results from a large, population-based survey confirm and extend findings of other, smaller-scale studies that plant- and fiber-rich dietary choices are associated with a more diverse and compositionally distinct microbiota, and with a greater potential to produce SCFAs.

The pathophysiology of psychiatric and neurodegenerative disorders is complex and multifactorial. Polyphenols possess a range of potentially beneficial mechanisms of action that relate to the implicated pathways in psychiatric and neurodegenerative disorders. The aim of this review is to highlight the emerging clinical trial and preclinical efficacy data regarding the role of polyphenols in mental and brain health, elucidate novel mechanisms of action including the gut microbiome and gene expression, and discuss the factors that may be responsible for the mixed clinical results; namely, the role of interindividual differences in treatment response and the potentially pro-oxidant effects of some polyphenols. Further clarification as part of larger, well conducted randomized controlled trials that incorporate precision medicine methods are required to inform clinical efficacy and optimal dosing regimens.

Clinical features of atopic dermatitis change with age as skin homeostatic mechanisms develop. In some cases, symptoms persist from childhood to adult. In early childhood, the characteristic features of this disease are eczema or exudative papules accompanied by itching. After childhood, lichenified dermatitis preceded by severe itching is the major skin manifestation. Presumably, this difference in clinical symptoms between childhood and adulthood may derive from the age-specific physiological function of skin, such as maintenance of proper stratum corneum, secretion of lipids, and perspiration. The volume and composition of secreted lipids and sweat change with age; these changes affect water retention, skin surface pH, and the microbiome. These physiological activities do not follow a hierarchy, but instead are coordinated to harmonize the maintenance of skin homeostasis. Thus, daily skin care based on the characteristic age-specific physiological function of skin should be considered to manage atopic dermatitis. The usage of moisturizers contributes to reduce skin dryness and the incidence of atopic dermatitis, and is recommended immediately after bathing. A water temperature of 38 to 40 degrees during bathing can be beneficial for barrier recovery, and gentle detergents or soap should be chosen if necessary. After exercise, excess sweat on the skin surface should be rinsed off. Avoidance of perspiration-inducing activities is not necessary. High temperature and humidity on skin surface may cause the development of miliaria and subsequent anhidrosis. Wearing hygroscopic and breathable underwear is recommended.

The gut microbiome is the main source of microorganisms for the formation of microbiomes of other organs and tissues. Dysbiosis of the intestine and lungs associated with COVID-19 leads to an increase in inflammatory reactions and stimulates the development of a cytokine storm through an increase in the activity of toll receptors. The patient’s intestinal dysbiosis facilitates the invasion of coronaviruses and intensifies inflammatory responses. Conversely, the progression of COVID-19 leads to increased dysbiosis in both the lungs and the intestines. Improving the microbiome through probiotic strains of bifido / lactobacilli and prebiotic substances is an important approach to mitigate the “wave” of COVID-19 at the population level.

Historically, the MISTEACHING (microbiome, immunity, sex, temperature, environment, age, chance, history, inoculum, nutrition, genetics) framework to describe the outcome of host−pathogen interaction, has been applied to human pathogens. Here, we show, using Actinobacillus pleuropneumoniae as an exemplar, that the MISTEACHING framework can be applied to a strict veterinary pathogen, enabling the identification of major research gaps, the formulation of hypotheses whose study will lead to a greater understanding of pathogenic mechanisms, and/or improved prevention/therapeutic measures. We also suggest that the MISTEACHING framework should be extended with the inclusion of a ‘strain’ category, to become MISTEACHINGS. We conclude that the MISTEACHINGS framework can be applied to veterinary pathogens, whether they be bacteria, fungi, viruses, or parasites, and hope to stimulate others to use it to identify research gaps and to formulate hypotheses worthy of study with their own pathogens.

The gut microbiome (GM) has been implicated in a vast number of human pathologies and has become a focus of oncology research over the past 5 years. The normal gut microbiota imparts specific function in host nutrient metabolism, xenobiotic and drug metabolism, maintenance of structural integrity of the gut mucosal barrier, immunomodulation and protection against pathogens. Strong evidence is emerging to support the effects of the GM on the development of some malignancies but also on responses to cancer therapies, most notably, immune checkpoint inhibition. Tools for manipulating the GM including dietary modification, probiotics and faecal microbiota transfer (FMT) are in development. Current understandings of the many complex interrelationships between the GM, cancer, the immune system, nutrition and medication are ultimately based on a combination of short‐term clinical trials and observational studies, paired with an ever-evolving understanding of cancer biology. The next generation of personalised cancer therapies focusses on molecular and phenotypic heterogeneity, tumour evolution and immune status; it is distinctly possible that the GM will become an increasingly central focus amongst them. The aim of this review is to provide clinicians with an overview of microbiome science and our current understanding of the role the GM plays in cancer.

The human gut harbors a dense and highly diverse microbiota of approximately 1,000 bacterial species. The interaction between the host and gut bacteria strongly influences human health. Numerous evidence suggest that intestinal flora imbalance is closely associated with the development and treatment of liver diseases, including acute liver injury and chronic liver diseases (cirrhosis, autoimmune liver disease, and fatty liver). Therefore, regulating the gut microbiota is expected to be a new method for the adjuvant treatment of liver diseases. Fecal microbiota transplantation (FMT) is defined as the transplantation of gut microbiota from healthy donors to sick patients via the upper or lower gastrointestinal route to restore the normal intestinal balance. In this study, we briefly review the current research on the gut microbiota and its link to liver diseases and then summarize the evidence to elucidate the clinical application and development of FMT in liver disease treatment.

Antigenic and metabolic integration of the intestinal microbiota into the homeostasis of the human body is a factor that claims to play a key role in the pathogenesis of cardiovascular diseases. It acquires special significance against the background of the decrease in blood circulation and congestion in the digestive system during chronic heart failure. Aim of the review is analysis and synthesis of studies results on the role of intestinal microbiocenosis in the pathogenesis of heart remodeling and chronic heart failure. The search for articles was conducted in databases eLIBRARY.RU and Medline for the key terms "gut microbiota (microbiome, microbiocenosis)", "dysbiosis (dysbacteriosis)", "excessive bacterial growth syndrome", "lipopolysaccharide (endotoxin)", "trimethylamine-N-oxide" in combination with the terms "heart failure", "myocardial remodeling", "myocardium" in Russian and English, respectively. We selected articles containing the results of clinical and experimental studies published from 1995 to 2020. Review articles were considered only on the subject of the cited original publications. Most researchers have established the relationship between chronic heart failure and dysfunction and changes in the qualitative and quantitative composition of intestinal microbiocenosis. As negative changes, it is customary to note the proliferation of gram-negative opportunistic bacteria with concomitant endotoxinemia and a decrease in the pool of commensal microbiota. The available data suggest that the participation of the intestinal microbial-tissue complex in the pathogenesis of chronic heart failure and heart remodeling is realized through the activation of a local and then systemic inflammatory response, accompanied by cardiodepressive action of pro-inflammatory cytokines and universal proliferation factors, an imbalance of matrix metalloproteinases and their inhibitors, the initiation of apoptosis, fibrosis, and loss of contractile myocardium. Besides, a decrease in the production of short-chain and polyunsaturated fatty acids and vitamins by the commensal microbiota may be associated with changes in the electrical properties of cardiomyocyte membranes, a decrease in the systolic function of the left ventricle of the heart, and an increase in the risk of sudden cardiac death. It's also shown that the direct cardiotoxic effect of microbial molecules (lipopolysaccharides, peptidoglycans, trimethylamine-N-oxide, etc.), which interact with the receptors of cardiomyocytes and microenvironment cells, can cause the development of myocardial remodeling and its dysfunction. Recent studies have established mechanisms of myocardial remodeling mediated by microbial molecules, which may be associated with new strategies for the treatment and prevention of heart failure.

Baboons inform on human gut microbiota Commensal bacteria are found throughout an organism, but it is not known whether associations between gut bacteria and their host are heritable. Grieneisen et al. examined changes in the microbiomes of 585 wild baboons from fecal samples collected over 14 years (see the Perspective by Cortes-Ortiz and Amato). Almost all microbiome traits tested demonstrated some level of statistically significant heritability. Most heritability values were low but varied over time correlating with the age of the host. Baboons live in an environment similar to that postulated for early humans and have a microbiome similar to that of humans. Thus, this heritability of the microbiome may reflect similar genetic determinants in humans, for which similar datasets are not available. Science , aba5483, this issue p. 181 ; see also abj5287, p. 159

Bile acids and their signaling pathways are increasingly recognized as potential therapeutic targets for cholestatic and metabolic liver diseases. This review summarizes new insights in bile acid physiology, focusing on regulatory roles of bile acids in the control of immune regulation and on effects of pharmacological modulators of bile acid signaling pathways in human liver disease. Recent mouse studies have highlighted the importance of the interactions between bile acids and gut microbiome. Interfering with microbiome composition may be beneficial for cholestatic and metabolic liver diseases by modulating formation of secondary bile acids, as different bile acid species have different signaling functions. Bile acid receptors such as FXR, VDR, and TGR5 are expressed in a variety of cells involved in innate as well as adaptive immunity, and specific microbial bile acid metabolites positively modulate immune responses of the host. Identification of Cyp2c70 as the enzyme responsible for the generation of hydrophilic mouse/rat-specific muricholic acids has allowed the generation of murine models with a human-like bile acid composition. These novel mouse models will aid to accelerate translational research on the (patho)physiological roles of bile acids in human liver diseases .

SARS-CoV-2 is the virus causing the major pandemic facing the world today. Although, SARS-CoV-2 primarily causes lung infection, a variety of symptoms have proven a systemic impact on the body. SARS-CoV-2 has spread in the community quickly infecting humans from all age, ethnicities and gender. However, fatal outcomes have been linked to specific host factors and co-morbidities such as age, hypertension, immuno-deficiencies, chronic lung diseases or metabolic disorders. A major shift in the microbiome of patients suffering of the coronavirus disease 2019 (COVID-19) have also been observed and is linked to a worst outcome of the disease. As many co-morbidities are already known to be associated with a dysbiosis of the microbiome such as hypertension, diabetes and metabolic disorders. Host factors and microbiome changes are believed to be involved as a network in the acquisition of the infection and the development of the diseases. We will review in detail in this manuscript, the immune response toward SARS-CoV-2 infection as well as the host factors involved in the facilitation and worsening of the infection. We will also address the impact of COVID-19 on the host’s microbiome and secondary infection which also worsen the disease.

Viral infections are known to modulate the upper respiratory tract microbiome, but few studies have addressed differences in the nasopharyngeal microbiome following SARS-CoV-2 infection. Using nasopharyngeal swab medical waste samples from 79 confirmed SARS-CoV-2 positive and 20 SARS-CoV-2 negative patients, we assessed microbiome composition with metagenomic sequencing. COVID-19 status and breathing assistive device use was associated with differences in beta diversity, principal component analyses, community composition and abundance of several species. Serratia more frequently appeared in COVID-19 patient samples compared to negative patient samples, and Serratia, Streptococcus, Enterobacter, Veillonella, Prevotella, and Rothia appeared more frequently in samples of those who used breathing assistive devices. Smoking and age were associated with differences in alpha diversity. Cross-sectional differences in the microbiome were apparent with SARS-CoV-2 infection, but longitudinal studies are needed to understand the dynamics of viral and breathing treatment modulation of microbes.

In this paper we discuss two universal characteristics of domesticated species that distinguish them from the wild closely related ancestors – increased socialization and phenotypic variability. Examining evidence accumulated in the literature up to date, we note that the gut microbiome is involved in the increased social behavior of domesticated species through the gut-immune system-brain axis. We further discuss data that point toward clear difference in the microbiome composition between domesticated species and closely related wild ancestors. This difference is related to changes in diet, due to co-habitation with humans, which leads to increase in Bifidobacteria and changes in carbohydrate metabolism. We note that these changes may also influence interaction between microbiome and virome. Virome is linked to the evolutionary changes through incorporation of retro-viruses into the host genome. Together with transposons these mobile genetic elements may also lead to changes in regulatory networks, and increase adaptive potential. Changes in microbiome of animals during co-habitation with humans should be considered as an important event during domestication process.

Lipodystrophic mice are protected from cartilage damage following joint injury. This protection can be reversed by the implantation of a small adipose tissue graft. The purpose of this study was to evaluate the relationship between the gut microbiota and knee cartilage damage while controlling for adiposity, high fat diet, and joint injury using lipodystrophic (LD) mice. LD and littermate control (WT) mice were fed a high fat diet, chow diet, or were rescued with fat implantation, then challenged with destabilization of the medial meniscus surgery to induce osteoarthritis (OA). 16S rRNA sequencing was conducted on feces. MaAslin2 was used to determine associations between taxonomic relative abundance and OA severity. While serum LPS levels between groups were similar, synovial fluid LPS levels were increased in both limbs of HFD WT mice compared to all groups, except for fat transplanted animals. The Bacteroidetes:Firmicutes ratio of the gut microbiota was significantly reduced in HFD and OA-rescued animals when compared to chow. Nine novel significant associations were found between gut microbiota taxa and OA severity. These findings suggest the presence of causal relationships the gut microbiome and cartilage health, independent of diet or adiposity, providing potential therapeutic targets through manipulation of the microbiome.

Background The role of intestinal microbiota in the pathogenesis of late-onset sepsis (LOS) in preterm infants is largely unexplored but could provide opportunities for microbiota-targeted preventive and therapeutic strategies. We hypothesized that microbiota composition changes before the onset of sepsis, with causative bacteria that are isolated later in blood culture. Methods This multicenter case-control study included preterm infants born under 30 weeks of gestation. Fecal samples collected from the 5 days preceding LOS diagnosis were analyzed using a molecular microbiota detection technique. LOS cases were subdivided into 3 groups: gram-negative, gram-positive, and coagulase-negative Staphylococci (CoNS). Results Forty LOS cases and 40 matched controls were included. In gram-negative LOS, the causative pathogen could be identified in at least 1 of the fecal samples collected 3 days prior to LOS onset in all cases, whereas in all matched controls, this pathogen was absent (P = .015). The abundance of these pathogens increased from 3 days before clinical onset. In gram-negative and gram-positive LOS (except CoNS) combined, the causative pathogen could be identified in at least 1 fecal sample collected 3 days prior to LOS onset in 92% of the fecal samples, whereas these pathogens were present in 33% of the control samples (P = .004). Overall, LOS (expect CoNS) could be predicted 1 day prior to clinical onset with an area under the curve of 0.78. Conclusions Profound preclinical microbial alterations underline that gut microbiota is involved in the pathogenesis of LOS and has the potential as an early noninvasive biomarker.

Recent studies identified specific gut microbial species linked to various human diseases, and gut-brain axis is currently attracting much attention in the field of microbiome science clinically and biologically. Research on multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis is one of the most active research subjects. Notably, recent achievements established the bidirectional causality between MS and gut microbiome. The reduction of gut microbiome-derived short chain fatty acids and the enrichment of gut-associated oxidative stress appear to be promoting for neurodegenerative processes. Also, researchers are trying to elucidate the mechanisms by which the microbiome regulates the onset and progression of MS. The new findings achieved by the analysis of the causal relationship between MS and the gut microbiome will provide a new therapeutic strategy for MS. These results will contribute to our understanding of the cause, prevention, and treatment of MS, and will lead to a complete cure for this disease in the future. In MS, for which no curative treatment has yet to be established, the unmet needs may be overcome through the analysis of gut microbiome.

The human oral and gut commensal microbes play vital roles in the development and maintenance of immune homeostasis, while its association with susceptibility and severity of SARS-CoV-2 infection is barely understood. In this study, we investigated the dynamics of the oral and intestinal flora before and after the clearance of SARS-CoV-2 in 53 COVID-19 patients, and then examined their microbiome alterations in comparison to 76 healthy individuals. A total of 140 throat swab samples and 81 fecal samples from these COVID-19 patients during hospitalization, and 44 throat swab samples and 32 fecal samples from sex and age-matched healthy individuals were collected and then subjected to 16S rRNA sequencing and viral load inspection. We found that SARS-CoV-2 infection was associated with alterations of the microbiome community in patients as indicated by both alpha and beta diversity indexes. Several bacterial taxa were identified related to SARS-CoV-2 infection, wherein elevated Granulicatella and Rothia mucilaginosa were found in both oral and gut microbiome. The SARS-CoV-2 viral load in those samples was also calculated to identify potential dynamics between COVID-19 and the microbiome. These findings provide a meaningful baseline for microbes in the digestive tract of COVID-19 patients and will shed light on new dimensions for disease pathophysiology, potential microbial biomarkers, and treatment strategies for COVID-19.

Chemotherapy treatment is associated with acute behavioral side effects (fatigue, anorexia) that significantly reduce patient quality of life and are dose-limiting, thereby increasing mortality (Kidwell et al., 2014). Disruptions to gut homeostasis (diarrhea, constipation, microbial dysbiosis) are also observed in patients receiving chemotherapy. In non-oncological patients, facets of mental health (fatigue, anxiety, depression) correlate with alterations in the gut microbiome, suggestive of a contribution of the gut in CNS disease etiology. The potential gut-to-brain pathway is poorly understood in patients receiving chemotherapy. Our prior studies have demonstrated a correlation between chemotherapy treatment, gut changes, peripheral and central inflammation, and behavioral symptoms in mice. Here we aimed to determine the extent to which chemotherapy-associated gut manipulations modulate the behavioral and biological consequences of chemotherapy. We measured sickness behaviors, peripheral and central inflammatory mediators, and anxiety in conventional or germ-free female mice: 1) cohabitating with mice of the opposite treatment group, 2) pre-treated with broad-spectrum antibiotics, or 3) given an intra-gastric gavage of gut content from chemotherapy-treated mice. In cohabitation studies, presumed coprophagia promoted body mass recovery, however strong associations with inflammation and behavior were not observed. Reduction of gut microbial alpha diversity via antibiotics did not prevent chemotherapy-associated side effects, however the relative abundances of the genera Tyzzerella, Romboutsia, and Turicibacter correlated with circulating inflammatory (IL-1β) and behavioral outcomes (lethargy, anxiety-like behavior). A gut microbiota transplant from chemotherapy-treated mice decreased central locomotion in open field testing, increased circulating CXCL1, and increased hippocampal Il6 and Tnfa in germ-free mice compared to germ-free mice that received a transplant from vehicle-treated mice. Taken together, these data provide further evidence that the gut microbiota likely contributes to the development of chemotherapy-associated side effects. This work has significant implications in the future treatment of anxiety in patients, and warrants future studies using microbe-based treatment options.