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Background Intestinal microbiota might interact with capecitabine and vice versa. Patients and methods 33 mCRC patients collected faecal samples before, during, and after three cycles capecitabine. Results Intestinal microbiota were not affected by capecitabine and not different between responders and non-responders. Conclusions Our study provides insights into challenges and points of attention for the design of upcoming clinical microbiota studies. Background Previous pre-clinical research has indicated that the intestinal microbiota can potentiate anti-tumour efficacy of capecitabine and that capecitabine treatment impacts intestinal microbiota composition and diversity. Using a longitudinal design, this study explores the associations between the intestinal microbiota and treatment response in patients with metastatic colorectal cancer (mCRC) during capecitabine treatment. Patients and methods Patients with mCRC treated with capecitabine were prospectively enrolled in a multicentre cohort study. Patients collected a faecal sample and completed a questionnaire before, during, and after three cycles of capecitabine. Several clinical characteristics, including tumour response, toxicity and antibiotic use were recorded. Intestinal microbiota were analysed by amplicon sequencing of the 16S rRNA V4 gene-region. Results 33 patients were included. After three cycles of capecitabine, six patients (18%) achieved a partial response, 25 (76%) showed stable disease, and one (3%) experienced progressive disease. 90 faecal samples were collected. Microbial diversity (α-diversity), community structure (β-diversity), and bacterial abundance on phylum and genus level were not significantly different between responders and non-responders and were not significantly affected by three cycles of capecitabine. Conclusions This is the first clinical study with longitudinal intestinal microbiota sampling in mCRC patients that explores the role of the intestinal microbiota during treatment with capecitabine. Intestinal microbiota composition and diversity before, during, and after three cycles of capecitabine were not associated with response in this study population. Capecitabine did not induce significant changes in the microbiota composition and diversity during the treatment period. Individual effects of antibiotics during capecitabine treatment were observed.

People are increasingly aware of the role of vegetarian diets in modulating human gut microbial abundance and intestinal physiology. A plant-based diet is thought to benefit host health by contributing to establish a diverse and stable microbiome. In addition, microbe-derived metabolites of specific nutrients known to be abundant in vegetarian diets (such as indigestible carbohydrates, arginine, and others) are important to promote effective intestinal immune responses, maintain intestinal barrier function, and protect against pathogens. This review explores the characteristics of the gut microbiome formed by vegetarian diets and the effects of diet-associated nutrients on intestinal microbial abundance. The interactions between the microbe-derived metabolites of vegetarian diet-associated nutrients and intestinal physiology are also discussed.

SCFA increase serotonin (5-hydroxytryptamine, 5-HT) synthesis and content in the colon in vitro and ex vivo, but little is known in vivo. We tested whether dietary indigestible saccharides, utilised as a substrate to produce SCFA by gut microbiota, would increase colonic 5-HT content in mice. Male C57BL/6J mice were fed a purified diet and water supplemented with 4 % (w/v) 1-kestose (KES) for 2 weeks. Colonic 5-HT content and enterochromaffin (EC) cell numbers were lower in mice supplemented with KES than those without supplementation, while monoamine oxidase A activity and mRNA levels of tryptophan hydroxylase 1 (Tph1), chromogranin A (Chga), Slc6a4 and monoamine oxidase A (Maoa) genes in the colonic mucosa, serum 5-HT concentration and total 5-HT content in the colonic contents did not differ between groups. Caecal acetate concentration and Bifidobacterium pseudolongum population were higher in KES-supplemented mice. Similar trends were observed in mice supplemented with other indigestible saccharides, that is, fructo-oligosaccharides, inulin and raffinose. Intragastric administration of live B. pseudolongum (108 colony-forming units/d) for 2 weeks reduced colonic 5-HT content and EC cell numbers. These results suggest that changes in synthesis, reuptake, catabolism and overflow of 5-HT in the colonic mucosa are not involved in the reduction of colonic 5-HT content by dietary indigestible saccharides in mice. We propose that gut microbes including B. pseudolongum could contribute to the reduction of 5-HT content in the colonic mucosa via diminishing EC cells.

Background Age‐related muscle dysfunctions are common disorders resulting in poor quality of life in the elderly. Probiotic supplementation is a potential strategy for preventing age‐related sarcopenia as evidence suggests that probiotics can enhance muscle function via the gut–muscle axis. However, the effects and mechanisms of probiotics in age‐related sarcopenia are currently unknown. In this study, we examined the effects of Lactobacillus casei Shirota (LcS), a probiotic previously reported to improve muscle function in young adult mice. Methods We administered LcS (1 × 108 or 1 × 109 CFU/mouse/day) by oral gavage to senescence‐accelerated mouse prone‐8 mice for 12 weeks (16‐ to 28‐week‐old). Sixteen‐week‐old and 28‐week‐old SMAP8 mice were included as non‐aged and aged controls, respectively. Muscle condition was evaluated using dual‐energy X‐ray absorptiometry for muscle mass, holding impulse and grip strength tests for muscle strength, and oxygen consumption rate, gene expressions of mitochondrial biogenesis, and mitochondrial number assays for mitochondria function. Inflammatory cytokines were determined using enzyme‐linked immunosorbent assay. Gas chromatography–mass spectrometry was utilized to measure the short‐chain fatty acid levels. The gut microbiota was analysed based on the data of 16S rRNA gene sequencing of mouse stool. Results The LcS supplementation reduced age‐related declines in muscle mass (>94.6%, P 66% in holding impulse and >96.3% in grip strength, P 65.9% in the mice given high dose of LcS, P 89.4%, P 2.0] were positively correlated with healthy muscle and physiological condition (P 2.0) were negatively associated with healthy muscle and physiological condition (P

This research aimed to investigate the antidiabetic activity, underlying mechanisms, and gut microbiota regulation of aloin. The insulin-resistant HepG2 (IR-HepG2) cell model and the type 2 diabetic (T2D) mouse model were successfully established using dexamethasone and a high-fat high-sucrose diet with low-dose streptozotocin, respectively. Aloin intervention increased glucose consumption and stimulated the activity of hexokinase and pyruvate dehydrogenase in IR-HepG2 cells. Additionally, it diminished the weight loss, reduced fasting blood glucose levels and hemoglobin A1c activity, and promoted glucose tolerance and fasting serum insulin activity in T2D mice. Histopathological analysis of the liver indicated hepatic protection by aloin. Additionally, aloin treatment inhibited the protein expression of c-Jun N-terminal kinases and activated that of IRS1/PI3K/Akt in the liver. Moreover, aloin modulated the bacterial community in the gut by raising the abundance of Bacteroidota and reducing the richness of Firmicutes, Proteobacteria, and Actinobacteriota. Thus, aloin ameliorated IR via activating IRS1/PI3K/Akt signaling pathway and regulating the gut microbiota, and it may be promising candidate as functional food for diabetic therapy.

Recently, pectin has been used as an alternative for commercial prebiotic products to modulate gut microbiota. In this study, the standard diet (Chow group) and high fat diet containing 0% (HF group), 1%, 3%, 5%, 8% or 12% (m/m) apple pectin (HF-P group) were offered ad libitum for 8 weeks to 4-week C57BL/6J mice (n = 10/group). Results showed that body weight gain (R2 = –0.990), subcutaneous adipose accumulation (R2 = –0.930), serum triglyceride elevation (R2 = –0.879), acetate (R2 = 0.955) and propionate concentration reduction (R2 = 0.985) were suppressed by pectin from 1% to 12%, indicating dose response to pectin consumption. Moreover, abundance of obesity-related bacteria Coriobacteriaceae, and pectin-degradating bacteria, Faecalibaculum, Ruminococcus were significantly increased with pectin dosage increased, and the R2 were 0.936, 0.963 and 0.937, respectively. Besides, attenuations for colonic injury and liver steatosis were observed after adding 5% and 8% pectin, respectively. This study confirmed the dose-sensitive manner of pectin to alleviate HF-induced obesity by modulating gut microbiota and enhancing short-chain fatty acids production.

Hepatic ischemia/reperfusion injury (HIRI) is a serious complication that occurs following shock and/or liver surgery. Gut microbiota and their metabolites are key upstream modulators of development of liver injury. Herein, we investigated the potential contribution of gut microbes to HIRI. Ischemia/reperfusion surgery was performed to establish a murine model of HIRI. 16S rRNA gene sequencing and metabolomics were used for microbial analysis. Transcriptomics and proteomics analysis were employed to study the host cell responses. Our results establish HIRI was significantly increased when surgery occurred in the evening (ZT12, 20:00) when compared with the morning (ZT0, 08:00); however, antibiotic pretreatment reduced this diurnal variation. The abundance of a microbial metabolite 3,4-dihydroxyphenylpropionic acid was significantly higher in ZT0 when compared with ZT12 in the gut and this compound significantly protected mice against HIRI. Furthermore, 3,4-dihydroxyphenylpropionic acid suppressed the macrophage pro-inflammatory response in vivo and in vitro. This metabolite inhibits histone deacetylase activity by reducing its phosphorylation. Histone deacetylase inhibition suppressed macrophage pro-inflammatory activation and diminished the diurnal variation of HIRI. Our findings revealed a novel protective microbial metabolite against HIRI in mice. The potential underlying mechanism was at least in part, via 3,4-dihydroxyphenylpropionic acid-dependent immune regulation and histone deacetylase (HDAC) inhibition in macrophages.

In the present study, an oligosaccharide SPO-1 from Spirulina platensis was prepared by glycosidase from a marine bacterium. The prebiotic activity of SPO-1 on the growth of Lactobacillus paracasei and Bifidobacterium animalis, and its effect on human gut microbiota were examined in vitro. The molecular weight of the tetrasaccharide SPO-1 was 650.2 Da, and it was mainly composed of glucose with α-type glycosidic linkages. The prebiotic activity score of SPO-1 was the highest for the growth of probiotic strains L. paracasei and B. animalis. Furthermore, as fermentation proceeded, SPO-1 was gradually degraded and utilized by intestinal bacteria. The results showed that after treatment with SPO-1, carbohydrate consumption and short-chain fatty acids levels were increased, especially those of i-butyric and i-valeric acids. Moreover, SPO-1 significantly promoted the abundance, diversity and composition of gut microbiota, especially stimulating the growth of Bacteroides, Escherichia-Shigella and Megamonas. In addition, the change in intestinal microbiota function predicted by phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt) after treatment with SPO-1 is mainly related to the terms “carbohydrate metabolism” and “amino acid metabolism”. These results suggest that SPO-1 is a potential oligosaccharide in regulation of intestinal microbiota.

Grifola frondosa polysaccharide (GFP) as the natural compounds have been reported to exert diverse bioactivities. The aim of this study was to investigate the regulatory effects of GFP on intestinal microbiota in type 2 diabetic mice. The changes of microbiota in faeces of the diabetic mice upon high fat diet were determined and the V3 region of the 16S rRNA was sequenced by Illumina MiSeq high-throughput sequencing platform. Eighty operational taxonomic unit were identified to be shared by all samples, and the quality and richness of sequencing were assessed via rarefaction and rank abundance curves. The diversity of gut flora was slightly improved in diabetic mice after GFP treatment. The composition and relative abundance of gut microbiota at phylum and genus levels were altered by GFP. The abundance of Robinsoniella, Flavonifractor, Anaerotruncus, and Desulfvibrio were found to concentrate on diabetic mice through LEfSe analysis. Furthermore, Alloprevotella and Burkholderia had strong relevancy with other gut flora. Based on the findings, GFP might be a desired candidate on ameliorating the intestinal unbalance in diabetes.

Phosphodiesterase-4 (PDE4) functions as a catalyzing enzyme targeting hydrolyzation of intracellular cyclic adenosine monophosphate (cAMP) and inhibition of PDE4 has been proven to be a competitive strategy for dermatological and pulmonary inflammation. However, the pathological role of PDE4 and the therapeutic feasibility of PDE4 inhibitors in chronic ulcerative colitis (UC) are less clearly understood. This study introduced apremilast, a breakthrough in discovery of PDE4 inhibitors, to explore the therapeutic capacity in dextran sulfate sodium (DSS)-induced experimental murine chronic UC. In the inflamed tissues, overexpression of PDE4 isoforms and defective cAMP-mediating pathway were firstly identified in chronic UC patients. Therapeutically, inhibition of PDE4 by apremilast modulated cAMP-predominant protein kinase A (PKA)–cAMP-response element binding protein (CREB) signaling and ameliorated the clinical symptoms of chronic UC, as evidenced by improvements on mucosal ulcerations, tissue fibrosis, and inflammatory infiltrations. Consequently, apremilast maintained a normal intestinal physical and chemical barrier function and rebuilt the mucosal homeostasis by interfering with the cross-talk between human epithelial cells and immune cells. Furthermore, we found that apremilast could remap the landscape of gut microbiota and exert regulatory effects on antimicrobial responses and the function of mucus in the gut microenvironment. Taken together, the present study revealed that intervene of PDE4 provided an infusive therapeutic strategy for patients with chronic and relapsing UC., Graphical abstract Inhibition of PDE4 by apremilast ameliorated the clinical symptoms of experimental chronic UC through remapping the landscape of gut microbiota and rebuilding the mucosal homeostasis.Image 1

There are a number of health benefits of Mesona chinensis Benth polysaccharide (MP), but little is known about its hepatoprotective effect and effect on gut microbiota composition in mice with liver damage induced by cyclophosphamide (CTX). This study indicated that MP supplementation effectively inhibited the production of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT), enhanced liver antioxidant capacity and repaired liver damage in mice caused by CTX. The release of inflammatory cytokines in liver and the concentration of lipopolysaccharide (LPS) in serum were decreased, and the level of short chain fatty acids (SCFAs) in colon was increased after MP administration. Those effects may be correlated with the regulation of the gut microbiota. Importantly, MP restrained liver inflammatory responses induced by CTX may via increasing the SCFAs-producing bacteria family Ruminococcaceae and reduced LPS-producing bacteria genus Bacteroides. In short, the prevention of CTX-induced liver injury by supplementing MP is achieved at least in part by regulating the community structure of the gut microbiota, and MP is expected to be a potential prebiotic to treat and prevent liver diseases.

Background To reveal the changes of intestinal microbial abundance and composition, as well as the microbiota metabolic levels of bile acids and short chain fatty acids of healthy preschool children during their growth. Methods Feces of 120 healthy newborns and 150 healthy children aged 6 months to 6 years were collected. Then the composition of intestinal flora was analyzed by 16S rRNA, and the contents of bile acids and short chain fatty acids in feces were detected by LC-MS and GS methods, respectively. Results The composition and function of intestinal microflora were not stable in neonatal period but significantly improved at 6 months after birth, and gradually stabilized and tended to adult-like formation after 2–3 years old. The levels of short chain fatty acids and secondary bile acids were consistent with the development of gut microbiota. Conclusion The age of 6 months may be a critical period for the development of intestinal microflora in children.

There is an increasing recognition of the strong links between the gut microbiome and the brain, and there is persuasive evidence that the gut microbiome plays a role in a variety of physiological processes in the central nervous system. This review summarizes findings that gut microbial composition alterations are linked to hippocampal neurogenesis, as well as the possible mechanisms of action; the existing literature suggests that microbiota influence neurogenic processes, which can result in neurological disorders. We consider this evidence from the perspectives of neuroinflammation, microbial-derived metabolites, neurotrophins, and neurotransmitters. Based on the existing research, we propose that the administration of probiotics can normalize the gut microbiome. This could therefore also represent a promising treatment strategy to counteract neurological impairment.

Flaxseed has displayed the potential beneficial as functional foods. However, most studies focused on effects of flaxseed extracts or ingredients in flaxseed. Besides, few studies showed that flaxseed extracts contributed to anti-type 1 diabetes (T1D), yet the underlying mechanism is still unknown. In the present study, 16.7% of milled flaxseed (MF)-added diet was given to diabetic mice induced by streptozocin for 6 weeks. The results showed that MF feeding 1) slightly decreased blood glucose levels and improved the ability of glucose tolerance by oral glucose tolerance test, 2) decreased liver tumor necrosis factor-α levels and increased liver glycogen levels with significance via down-regulating TLR4/NF-κB pathways, 3) and significantly altered some beneficial bacteria in gut microbiota. In conclusion, the present study showed that milled flaxseed showed the potential on anti-T1D through anti-inflammation via TLR4/NF-κB and altering the gut microbiota in STZ-induced diabetic mice.

Torreya grandis cv. Merrillii (Taxace, Torreya) is mainly distributed across the hilly areas of subtropical China and is well known for its nutritional value. In this study, the ameliorative effects of T. grandis seed oil on lipid metabolism were investigated, and the underlying mechanism was explored from the perspective of gut microbiota. Mice experiments showed that the rate of body mass gain in the group where the mice were fed a high-fat diet (HFD) and supplemented with 550 mg/(kg·day) T. grandis seed oil (HFD + TO550 group) was 42.27%, while it was 62.25% in the HFD group. Compared with the HFD group, the liver and fat indices, total cholesterol, triglycerides, and low-density lipoprotein cholesterol were reduced in the oil-supplement groups. Moreover, the oil supplement significantly changed the fatty acid composition and alleviated pathological damage to the liver caused by the high-fat diet. Additionally, the distinct clustering of bacteria in the composition of gut microbiota was observed in the oil treatment group compared with that in the HFD group. T. grandis seed oil significantly increased the abundance of the beneficial bacteria and short-chain fatty acid producers, including Lactobacillus, Bifidobacterium, Faecalibaculum and Allobaculum. Our results suggest that the supplements of T. grandis seed oil could alleviate hyperlipidemia caused by HFD. These positive effects are considered to be related with sciadonic acid (SCA) and are partially mediated by alterations in gut microbiota composition and functionality.

Foxtail millet (FM) whole grain has received special attention in recent years. To confirm the hypoglycemic effects of FM, we investigated the effects of FM supplementation on glucose metabolism and gut microbiota in rats with high-fat diet/streptozotocin (HFD/STZ)-induced diabetes. Specifically, we fully assessed the blood biochemical profiles, pancreatic histopathology, insulin-glucagon immunofluorescence, short-chain fatty acids, and gut microbiota composition of rats with HFD/STZ-induced diabetes before and after FM supplementation. Results showed that both 30% and 48% FM supplementation significantly decreased concentrations of fasting blood glucose, 60-min blood glucose, and blood triglycerides (P

The metabolic syndrome (MS) has become one of the main problems in public health. Tea polyphenols (TPs), the main bioactive components of tea, has been claimed to have the potential to regulate metabolism and effectively prevent or mitigate the MS. However, many studies into the effects of TPs on MS have provided conflicting findings and the underlying mechanism has been elusive. The predominant TPs in unfermentedand and fermented tea are catechins and oxidized polyphenols (theaflavins and thearubigins), both of which have low bioavailability and reach the colon where most gut microbes inhabit. Gut microbiota has been demonstrated to be tightly associated with host metabolism. The interactions between TPs and gut microbiota will lead to the alterations of gut microbiota composition and the production of metabolites including short chain fatty acids, bile acids, amino acids and TPs derived metabolites, accordingly exerting their biological effects both locally and systemically. This review highlighted the contribution of metabolites and specific gut bacteria in the process of TPs intervention on the MS and further discuss how TPs impact the MS via gut microbiota from the viewpoint of gut organ/tissue axis.

The study was aimed to assess impact of high fat diet (HFD) and synthetic human gut microbiota (GM) combined with HFD and chow diet (CD) in inducing type-2 diabetes (T2D) using mice model. To our knowledge, this is the first study using selected human GM transplantation via culture based method coupled dietary modulation in mice for in vivo establishment of inflammation leading to T2D and gut dysbiosis. Twenty bacteria (T2D1-T2D20) from stool samples of confirmed T2D subjects were found to be morphologically different and subjected to purification on different media both aerobically and anerobically, which revealed seven bacteria more common among 20 isolates on the basis of biochemical characterization. On the basis of 16S rRNA gene sequencing, these seven isolates were identified as Bacteroides stercoris (MT152636), Lactobacillus acidophilus (MT152637), Lactobacillus salivarius (MT152638), Ruminococcus bromii (MT152639), Klebsiella aerogenes (MT152640), Bacteroides fragilis (MT152909), Clostridium botulinum (MT152910). The seven isolates were subsequently used as synthetic gut microbiome (GM) for their role in inducing T2D in mice. Inbred strains of albino mice were divided into four groups and were fed with CD, HFD, GM+HFD and GM+CD. Mice receiving HFD and GM+modified diet (CD/HFD) showed highly significant (P

Background Rotavirus (RV) is a principal cause of diarrhea. However, there is a limited understanding regarding alteration of the gut microbial community structure and abundance during RV infection. This study was to characterize any potential associations between RV infection and the intestinal microbiota. Methods Suckling mice were divided into normal group (NC) and infected group (RV) randomly. All of the suckling mice were euthanized four days post-RV infection. The virus titer was counted as fluorescent focus assay, and viral load was quantified by QPCR. Five sucking mice were randomly selected from each RV group and NC group for sample collection and pathological analysis. Mixed intestinal contents of the colon and rectum were collected from all of the suckling mice. To investigate the detailed relationship between RV infection and intestinal microbiota, the composition and distribution of intestinal microbiota from suckling mice were first analyzed using 16S rRNA sequencing technology. Results The results of the pathological characteristics showed that vacuolar degeneration, vasodilation, hyperemia, and destruction of the intestinal epithelium were apparent in the RV group. Representative genera from Lactobacillus and Fusobacterium were enriched in the NC group, while the Enterococcus and Escherichia/Shigella genera were enriched in the RV group. Helicobacter, Alloprevotrlla, Brevundimonas, Paenibacillus, and Parabacteroides were completely undetectable in the RV group. The predicted intestinal flora metabolic function results showed that “carbohydrate metabolism” and “lipid metabolism” pathways were significantly enriched within the NC group. A significant difference has been observed in the gut microbiota composition between the two groups. Conclusions Our results demonstrated a significant difference in the gut microbiota composition in RV-infected suckling mice as compared to the RV un-infected suckling mice group. This work may provide meaningful information regarding the bacterial genera changed during RV infection. Moreover, the changes in these bacteria may be related with the replication and pathogenesis of RV infection.

Background Cancer cachexia is a multifactorial metabolic syndrome in which bile acid (BA) metabolism might be involved. The aim of the present study was to clarify the contribution of liver and gut microbiota to BA metabolism disturbance in cancer cachexia and to check the possibility of targeting BA metabolism using agents such as tauroursodeoxycholic acid (TUDCA) for cancer cachexia therapy. Methods The BA profiles in liver, intestine, and serum of mice with cancer cachexia induced by inoculation of colon C26 tumour cells were analysed using metabolomics methods and compared with that of control mice. Proteomic analysis of liver protein expression profile and 16S rRNA gene sequencing analysis of gut microbiota composition in cancer cachexia mice were conducted. Expression levels of genes related to farnesoid X receptor (FXR) signalling pathway in the intestine and liver tissues were analysed using RT–PCR analysis. The BA profiles in serum of clinical colon cancer patients with or without cachexia were also analysed and compared with that of healthy volunteers. The effects of TUDCA in treating cancer cachexia mice were observed. Results In the liver of cancer cachexia mice, expression of BA synthesis enzymes was inhibited while the amount of total BAs increased (P

Changes in the microbiota are associated with alterations in nervous system structure-function and behavior and have been implicated in the etiology of neuropsychiatric and neurodegenerative disorders. Most of these studies have centered on mammalian models due to their phylogenetic proximity to humans. Indeed, the germ-free mouse has been a particularly useful model organism for investigating microbiota-brain interactions. However, microbiota-brain axis research on simpler genetic model organisms with a vast and diverse scientific toolkit (zebrafish, Drosophila melanogaster, and Caenorhabditis elegans) is now also coming of age. In this review, we summarize the current state of microbiota-brain axis research in rodents and humans, and then we elaborate and discuss recent research on the neurobiological and behavioral effects of the microbiota in the model systems of fish, flies, and worms. We propose that a cross-species, holistic and mechanistic approach to unravel the microbiota-brain communication is an essential step toward rational microbiota-based therapeutics to combat brain disorders.

Background Gut microbiota dysbiosis and sarcopenia commonly occur in the elderly. Although the concept of the gut–muscle axis has been raised, the casual relationship is still unclear. This systematic review analyses the current evidence of gut microbiota effects on muscle/sarcopenia. Methods A systematic review was performed in PubMed, Embase, Web of Science, and The Cochrane Library databases using the keywords (microbiota* OR microbiome*) AND (sarcopen* OR muscle). Studies reporting the alterations of gut microbiota and muscle/physical performance were analysed. Results A total of 26 pre‐clinical and 10 clinical studies were included. For animal studies, three revealed age‐related changes and relationships between gut microbiota and muscle. Three studies focused on muscle characteristics of germ‐free mice. Seventy‐five per cent of eight faecal microbiota transplantation studies showed that the recipient mice successfully replicated the muscle phenotype of donors. There were positive effects on muscle from seven probiotics, two prebiotics, and short‐chain fatty acids (SCFAs). Ten studies investigated on other dietary supplements, antibiotics, exercise, and food withdrawal that affected both muscle and gut microbiota. Twelve studies explored the potential mechanisms of the gut–muscle axis. For clinical studies, 6 studies recruited 676 elderly people (72.8 ± 5.6 years, 57.8% female), while 4 studies focused on 244 young adults (29.7 ± 7.8 years, 55.4% female). The associations of gut microbiota and muscle had been shown in four observational studies. Probiotics, prebiotics, synbiotics, fermented milk, caloric restriction, and exercise in six studies displayed inconsistent effects on muscle mass, function, and gut microbiota. Conclusions Altering the gut microbiota through bacteria depletion, faecal transplantation, and various supplements was shown to directly affect muscle phenotypes. Probiotics, prebiotics, SCFAs, and bacterial products are potential novel therapies to enhance muscle mass and physical performance. Lactobacillus and Bifidobacterium strains restored age‐related muscle loss. Potential mechanisms of microbiome modulating muscle mainly include protein, energy, lipid, and glucose metabolism, inflammation level, neuromuscular junction, and mitochondrial function. The role of the gut microbiota in the development of muscle loss during aging is a crucial area that requires further studies for translation to patients.

Historically, intermittent fasting (IF) has been considered as an effective strategy for controlling the weight of athletes before competition. Along with excellent insight into its application in various spaces by numerous studies, increasing IF-mediated positive effects have been reported, including anti-aging, neuroprotection, especially obesity control. Recently, the gut microbiota has been considered as an essential manipulator for host energy metabolism and its structure has been reported to be sensitive to dietary structure and habits, indicating that there is a potential and strong association between IF and gut microbiota. In this paper, we focus on the crosstalk between these symbionts and energy metabolism during IF which hold the promise to optimize host energy metabolism at various physical positions, including adipose tissue, liver and intestines, and further improve milieu internal homeostasis. Moreover, this paper also discusses the positive function of a potential recommendatory strain (Akkermansia muciniphila) based on the observational data for IF-mediated alternated pattern of gut microbiota and a hopefully regulatory pathway (circadian rhythm) for gut microbiota in IF-involved improvement on host energy metabolism. Finally, this review addresses the limitation and perspective originating from these studies, such as the association with tissue-specific bio-clock and single strain research, which may continuously reveal novel viewpoints and mechanisms to understand the energy metabolism and develop new strategies for treating obesity, diabetes, and metabolic disorders.

Liver cancer is a leading cause of death worldwide, and hepatocellular carcinoma (HCC) is the most frequent primary liver tumour, followed by cholangiocarcinoma. Notably, secondary tumours represent up to 90% of liver tumours. Chronic liver disease is a recognised risk factor for liver cancer development. Up to 90% of the patients with HCC and about 20% of those with cholangiocarcinoma have an underlying liver alteration. The gut microbiota-liver axis represents the bidirectional relationship between gut microbiota, its metabolites and the liver through the portal flow. The interplay between the immune system and gut microbiota is also well-known. Although primarily resulting from experiments in animal models and on HCC, growing evidence suggests a causal role for the gut microbiota in the development and progression of chronic liver pathologies and liver tumours. Despite the curative intent of "traditional" treatments, tumour recurrence remains high. Therefore, microbiota modulation is an appealing therapeutic target for liver cancer prevention and treatment. Furthermore, microbiota could represent a non-invasive biomarker for early liver cancer diagnosis. This review summarises the potential role of the microbiota and immune system in primary and secondary liver cancer development, focusing on the potential therapeutic implications.

Coronavirus disease 2019 (COVID-19) is a disease produced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and it is currently causing a catastrophic pandemic affecting humans worldwide. This disease has been lethal for approximately 3.12 million people around the world since January 2020. Globally, among the most affected countries, Mexico ranks third in deaths after the United States of America and Brazil. Although the high number of deceased people might also be explained by social aspects and lifestyle customs in Mexico, there is a relationship between this high proportion of deaths and comorbidities such as high blood pressure (HBP), type 2 diabetes, obesity, and metabolic syndrome. The official epidemiological figures reported by the Mexican government have indicated that 18.4% of the population suffers from HBP, close to 10.3% of adults suffer from type 2 diabetes, and approximately 36.1% of the population suffers from obesity. Disbalances in the gut microbiota (GM) have been associated with these diseases and with COVID-19 severity, presumably due to inflammatory dysfunction. Recent data about the association between GM dysbiosis and metabolic diseases could suggest that the high levels of susceptibility to SARS-CoV-2 infection and COVID-19 morbidity in the Mexican population are primarily due to the prevalence of type 2 diabetes, obesity, and metabolic syndrome.

The gastrointestinal (GI) system contains many different types of immune cells, making it a key immune organ system in the human body. In the last decade, our knowledge has substantially expanded regarding our understanding of the gut microbiome and its complex interaction with the gut immune system. Short chain fatty acids (SCFA), and specifically butyrate, play an important role in mediating the effects of the gut microbiome on local and systemic immunity. Gut microbial alterations and depletion of luminal butyrate have been well documented in the literature for a number of systemic and GI inflammatory disorders. Although a substantial knowledge gap exists requiring the need for further investigations to determine cause and effect, there is heightened interest in developing immunomodulatory therapies by means of reprogramming of gut microbiome or by supplementing its beneficial metabolites, such as butyrate. In the current review, we discuss the role of endogenous butyrate in the inflammatory response and maintaining immune homeostasis within the intestine. We also present the experimental models and human studies which explore therapeutic potential of butyrate supplementation in inflammatory conditions associated with butyrate depletion.

Anorexia nervosa (AN), an eating disorder, is characterized by extreme weight loss and fear of weight gain. Psychosocial factors are thought to play important roles in the development and progression of AN; however, biological factors also presumably contribute to eating disorders. Recent evidence has shown that the gut microbiota plays an important role in pathogenesis of neuropsychiatric disorders including AN. In this article, we describe the possible role of the gut microbiota in the development and persistence of AN, based on the latest research works, including those of our group.

Obesity is a multifactorial disease that leads to excessive adipose tissue accumulation, mainly visceral fat. Importance and prevalence of obesity has increased significantly in recent decades all over the world. Until now, the pandemic of obesity has been associated more to lifestyle changes: excessive eating and low physical activity. In recent years, special attention has been paid to studying of composition and functions of intestinal microbiota as major factor in development of obesity and related comorbidities, such as hypertension, cardiac ischemia, heart failure and others. It is proved that gut microbiota affects extraction, accumulation and consumption of energy derived from food, lipid metabolism and immune response. It is also revealed that composition of the microbiota is different in thin and obese people. Thus, study of the relationship between intestinal microbiota composition and risk factors for cardiovascular diseases, in particular obesity, is an actual task. The purpose of this review is analyzing of literature about assessment of relationship between composition and functions of intestinal microbiota in the diagnostics, prevention and treatment of obesity and cardiovascular diseases.

Background The spontaneous osteoarthritis (OA) in rhesus macaque is similar to OA in human, which maintains an upright body posture and shows very similar biomechanical properties of bones to humans. At present, there is no good treatment for OA. This study aims to explore relationship between OA and intestinal microbiota, and provide a reference for the treatment of clinical OA. Results We collected colonic contents of the 20 rhesus macaque (6–15 years old, female) for intestinal microbiota analysis by metagenomics sequencing, of which 10 were spontaneous OA monkeys and 10 were normal monkeys. Our results showed the diversity of gut microbiota in monkeys with OA was decreased compared to the normal monkeys (p = 0.16). Mollicutes, Tenericutes, Coprobacillus and Faecalitalea may be biomarkers for the monkeys of OA. Lactobacillus found significantly increased in OA monkeys. Prevotella and Ruminococcus were higher in the normal group than OA group. Zinc/manganese transport system permease protein (p = 0.0011) and Cyclopropane-fatty-acyl-phospholipid synthase (p = 0.0012) are a microbiota metabolic pathway related to cartilage production. Conclusions Our results indicate that the diversity and composition of intestinal microbiota in monkeys with OA are different compared to the normal monkeys. we have found microbes that may be a biomarker for the diagnosis of osteoarthritis. Functional analysis of the microbiota also predicts cartilage damage in the monkeys with osteoarthritis. Non-human primates are closely related to humans, so this study can provide a reference for the development of drugs for the treatment of OA.

Probiotics have demonstrated their high potential to treat and/or prevent various diseases including neurodegenerative disorders, cancers, cardiovascular diseases, and inflammatory diseases. Probiotics are also effective against multidrug-resistant pathogens and help maintain a balanced gut microbiota ecosystem. Accordingly, the global market of probiotics is growing rapidly, and research efforts to develop probiotics into therapeutic adjuvants are gaining momentum. However, because probiotics are living microorganisms, many biological and biopharmaceutical barriers limit their clinical application. Probiotics may lose their activity in the harsh gastric conditions of the stomach or in the presence of bile salts. Moreover, they easily lose their viability under thermal or oxidative stress during their preparation and storage. Therefore, stable formulations of probiotics are required to overcome the various physicochemical, biopharmaceutical, and biological barriers and to maximize their therapeutic effectiveness and clinical applicability. This review provides an overview of the pharmaceutical applications of probiotics and covers recent formulation approaches to optimize the delivery of probiotics with particular emphasis on various dosage forms and formulation technologies.

Background Microbial acquisition and development of the gut microbiota impact the establishment of a healthy host-microbes symbiosis. Compared with other animals, the eusocial bumblebees and honeybees possess a simple, recurring, and similar set of gut microbiota. However, all bee gut phylotypes have high strain-level diversity. Gut communities of different bee species are composed of host-specific groups of strains. The variable genomic regions among strains of the same species often confer critical functional differences, such as carbon source utilization, essential for the natural selection of specific strains. The annual bumblebee colony founded by solitary queens enables tracking the transmission routes of gut bacteria during development stages. Results Here, we first showed the changes in the microbiome of individual bumblebees across their holometabolous life cycle. Some core gut bacteria persist throughout different stages of development. Gut microbiota of newly emerged workers always resembles those of their queens, suggesting a vertical transmission of strains from queens to the newborn workers. We then follow the dynamic changes in the gut community by comparing strain-level metagenomic profiles of queen-worker pairs longitudinally collected across different stages of the nest development. Species composition of both queen and worker shifts with the colony’s growth, and the queen-to-worker vertical inheritance of specific strains was identified. Finally, comparative metagenome analysis showed clear host-specificity for microbes across different bee hosts. Species from honeybees often possess a higher level of strain variation, and they also exhibited more complex gene repertoires linked to polysaccharide digestion. Our results demonstrate bacterial transmission events in bumblebee, highlighting the role of social interactions in driving the microbiota composition. Conclusions By the community-wide metagenomic analysis based on the custom genomic database of bee gut bacteria, we reveal strain transmission events at high resolution and the dynamic changes in community structure along with the colony development. The social annual life cycle of bumblebees is key for the acquisition and development of the gut microbiota. Further studies using the bumblebee model will advance our understanding of the microbiome transmission and the underlying mechanisms, such as strain competition and niche selection.

Aims Despite the interest in the association of gut microbiota with bone health, limited population-based studies of gut microbiota and bone mineral density (BMD) have been made. Our aim is to explore the possible association between gut microbiota and BMD. Methods A total of 3,321 independent loci of gut microbiota were used to calculate the individual polygenic risk score (PRS) for 114 gut microbiota-related traits. The individual genotype data were obtained from UK Biobank cohort. Linear regressions were then conducted to evaluate the possible association of gut microbiota with L1-L4 BMD (n = 4,070), total BMD (n = 4,056), and femur total BMD (n = 4,054), respectively. PLINK 2.0 was used to detect the single-nucleotide polymorphism (SNP) × gut microbiota interaction effect on the risks of L1-L4 BMD, total BMD, and femur total BMD, respectively. Results We detected five, three, and seven candidate gut microbiota-related traits for L1-L4 BMD, total BMD, and femur BMD, respectively, such as genus Dialister (p = 0.004) for L1-L4 BMD, and genus Eisenbergiella (p = 0.046) for total BMD. We also detected two common gut microbiota-related traits shared by L1-L4 BMD, total BMD, and femur total BMD, including genus Escherichia Shigella and genus Lactococcus. Interaction analysis of BMD detected several genes that interacted with gut microbiota, such as phospholipase D1 ( PLD1) and endomucin ( EMCN) interacting with genus Dialister in total BMD, and COL12A1 and Discs Large MAGUK Scaffold Protein 2 ( DLG2) interacting with genus Lactococcus in femur BMD. Conclusion Our results suggest associations between gut microbiota and BMD, which will be helpful to further explore the regulation mechanism and intervention gut microbiota of BMD. Cite this article: Bone Joint Res 2021;10(11):734–741.

Type 2 diabetes mellitus (T2DM) is a widespread metabolic disease characterized by chronic hyperglycemia. Human microbiota, which is regarded as a “hidden organ”, plays an important role in the initiation and development of T2DM. In addition, anti-hyperglycemic agents and traditional Chinese medicine may affect the composition of gut microbiota and consequently improve glucose metabolism. However, the relationship between gut microbiota, T2DM and anti-hyperglycemic agents or traditional Chinese medicine is poorly understood. In this review, we summarized pre-clinical and clinical studies to elucidate the possible underlying mechanism. Some anti-hyperglycemic agents and traditional Chinese medicine may partly exert hypoglycemic effects by altering the gut microbiota composition in ways that reduce metabolic endotoxemia, maintain the integrity of intestinal mucosal barrier, promote the production of short-chain fatty acids (SCFAs), decrease trimethylamine-N-oxide (TMAO) and regulate bile acid metabolism. In conclusion, gut microbiota may provide some new therapeutic targets for treatment of patients with diabetes mellitus.

Background Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. There is accumulating evidence that link gut microbiota to symptomatology and pathophysiology of PD. The aim of this study was to describe the pattern of gut microbiota and its association with PD and identify the effect of environmental factors on gut microbiota. This case–control study included 46 patients diagnosed as Parkinson’s disease (PD) and 31 healthy volunteers age and sex matched. Detailed history including age of onset, duration of disease, environmental risk factors, diet data, treatment, Unified Parkinson’s Disease Rating Scale (UPDRS), and gastrointestinal tract (GIT) domain of Non‐Motor Symptoms Scale (NMSS) were assessed. After extraction of bacterial DNA from the fecal samples, bacterial abundance was quantified by qPCR using 16S rRNA group-specific primers. Results Significant high abundance of Clostridium cluster IV, Akkermansia, Bifidobacterium, and lactic acid bacteria were found in the PD group compared with the control group (P P P = 0.002), while no significant correlations between different gut microbiota and demographic, environment data, different rating scores or dominant type of PD. There was a significant negative correlation between the Bifidobacterium with the duration of illness (P = 0.012). Conclusion The present study highlighted a significant connection between PD and levels of certain types of gut microbiota, in support of a possible link between gut microbiota and a neurodegenerative cascade of PD.

BACKGROUND Graft-versus-host disease (GVHD) following liver transplantation (LT) is an unpredictable complication with poor outcome. However, consensus regarding the diagnosis and therapeutic regimen for the disease is yet lacking. The present study summarized the clinical experience on the diagnosis and treatment of acute GVHD (aGVHD) following LT and reviewed the pertinent literature. CASE SUMMARY Between January 1st, 2000 and December 31st, 2020, a total of 1053 LT were performed in the First Affiliated Hospital of Xi’an Jiaotong University. Six recipients developed aGVHD with clinical symptoms of fever, rash, diarrhea, and pancytopenia. The incidence of aGVHD was 0.57%. The median time from LT to the clinical presentation of aGVHD was 22.17 d. The median time from the beginning of the clinical symptom to histopathological diagnosis was 7.5 d. All six cases underwent treatment of immunosuppressant adjustment, corticosteroids, human normal immunoglobulin, and antithymocyte globulin/IL-2 antagonists. Despite intensive treatment strategies, 4 patients were deceased due to sepsis, multiple organ failure, and cerebral hemorrhage. The remaining two cases were discharged as treatment successfully. However, one died because of tuberculosis infection on the 6th month of follow-up, the other one was alive healthy during 30 mo of follow-up. CONCLUSION The rapid diagnosis of aGVHD is mainly based on the time from the first symptom, histopathological features, and the donor T-lymphocyte chimerism. Our cases report highlights massive corticosteroid therapy and age difference between donors and recipients could accelerate to aGVHD. Moreover, gut microbial interventions and donor-targeted serotherapy may provide novel therapeutics.

BACKGROUND Dementia is a chronic progressive neurological disease affecting millions of people worldwide, and represents a relevant economic burden for healthcare systems. Although its pathogenesis is still unknown, recent findings have reported that a dysregulated gut-brain axis communication, a fundamental relationship mediated by several host and microbial molecules, is associated with cognitive disorders. In addition, gut microbiota manipulation reduces neuroinflammation, improving cognitive function by restoring the functional gut-brain axis. AIM To better define the effects of probiotics, prebiotics, synbiotics, and fecal microbiota transplant (FMT) on cognitive function. METHODS We performed a literature search of human randomized clinical trials to examine the effects of the administration of probiotics, prebiotics, synbiotics, or FMT on cognition outcomes in healthy or sick people of every age, sex, and nationality. We systematically searched Embase, Medline/PubMed, Cochrane Library, central and clinicaltrials.gov databases with a combination of comprehensive terms related to cognition and gut microbiota manipulation. Then we carefully reviewed and synthesized the data by type of study design and setting, characteristics of the studied population, kind of intervention (strain type or mixture type, dosage, and frequency of administration), control treatment, inclusion and exclusion criteria, follow-up duration, and cognitive or memory outcomes. RESULTS After examining the titles and abstracts, the initial literature screening identified 995 articles, but we added 23 papers in our systematic review. The analyses of these selected studies highlighted that both probiotic supplementation and FMT improved cognitive function regardless of the type and posology of administration and the adopted cognitive tests and questionnaires. We found that most of the studies conducted in healthy people showed a significant positive effect of the intervention on at least one of the performed cognitive tests. Regarding unhealthy subjects, while FMT and especially probiotic administration had multiple beneficial effects on different cognitive functions, supplementation with prebiotics did not provide any cognitive improvement. CONCLUSION Probiotic supplementation and FMT may represent a promising strategy to restore gut eubiosis and enhance the cognitive functions of healthy people and patients with neurological disorders.

The prevalence of diabetes has increased rapidly throughout the world in recent years. Currently, approximately 463 million people are living with diabetes, and the number has tripled over the last two decades. Here, we describe the global epidemiology of diabetes in 2019 and forecast the trends to 2030 and 2045 in China, India, USA, and the globally. The gut microbiota plays a major role in metabolic diseases, especially diabetes. In this review, we describe the interaction between diabetes and gut microbiota in three aspects: probiotics, antidiabetic medication, and diet. Recent findings indicate that probiotics, antidiabetic medications, or dietary interventions treat diabetes by shifting the gut microbiome, particularly by raising beneficial bacteria and reducing harmful bacteria. We conclude that targeting the gut microbiota is becoming a novel therapeutic strategy for diabetes.

Sepsis is a state of host immune response triggered by virus or bacterial infection, in which the extent of regional and systemic inflammation and companion counter‐inflammatory reactions determines disease outcomes. Probiotics are known for the immunomodulatory effect on allergic disorders, but it is not clear whether the beneficiary effect extends to sepsis and increases survival. In this mouse model, we injected intraperitoneally lipopolysaccharides (LPS) to induce sepsis, and investigated whether the pretreatment of Lactobacillus rhamnosus GG (LGG) contributed to host survival and examined the alteration of the gut microbiota and blood cytokines/chemokines profile before sepsis induction. Four‐week‐old male BALB/c mice were divided into two groups: one group were fed daily with LGG as a dietary supplement for fourteen days, whereas the other group with sterile water. Before sepsis induction, some mice from each group were killed to collect stool in the intestine and blood for microbial metagenomic and cytokine/chemokine analyses, respectively, and the rest were monitored afterward for mortality. The relative abundance of several families in the gut microbiota after LGG treatment was altered as well as the ratio of Firmicutes/Bacteroidetes. In addition, several pro‐inflammatory cytokines such as G‐CSF, IL7, IL15, and MCP1 were lower in the LGG group than in the control group. The survival rate following LPS‐induced sepsis improved with LGG treatment. Our results indicated that dietary supplement of probiotic LGG improved survival from LPS‐induced sepsis, most likely through pre‐septic changes in the gut microbial constituents by LGG with reciprocal alteration of host immune system to a less reactive state to incoming pathogens., LGG as dietary supplement decreased the F/B ratio of the gut microbiota and down‐regulated several pro‐inflammatory cyto‐kines/chemokines, but also increased survival rate in response to experimental sepsis.

Diverse communities of symbiotic microbes inhabit the digestive systems of vertebrates and play a crucial role in animal health, and host diet plays a major role in shaping the composition and diversity of these communities. Here, we characterized diet and gut microbiome of fire salamander populations from three Belgian forests. We carried out DNA metabarcoding on fecal samples, targeting eukaryotic 18S rRNA of potential dietary prey items, and bacterial 16S rRNA of the concomitant gut microbiome. Our results demonstrated an abundance of soft-bodied prey in the diet of fire salamanders, and a significant difference in the diet composition between males and females. This sex-dependent effect on diet was also reflected in the gut microbiome diversity, which is higher in males than female animals. Proximity to human activities was associated with increased intestinal pathogen loads. Collectively, the data supports a relationship between diet, environment and intestinal microbiome in fire salamanders, with potential health implications.

Berberine (BBR) is an isoquinoline alkaloid extracted from Coptis chinensis that improves diabetes, hyperlipidemia and inflammation. Due to the low oral bioavailability of BBR, its mechanism of action is closely related to the gut microbiota. This study focused on the CYP51 enzyme of intestinal bacteria to elucidate a new mechanism of BBR transformation by demethylation in the gut microbiota through multiple analytical techniques. First, the docking of BBR and CYP51 was performed; then, the pharmacokinetics of BBR was determined in ICR mice in vivo, and the metabolism of BBR in the liver, kidney, gut microbiota and single bacterial strains was examined in vitro. Moreover, 16S rRNA analysis of ICR mouse feces indicated the relationship between BBR and the gut microbiota. Finally, recombinant E. coli containing cyp51 gene was constructed and the CYP51 enzyme lysate was induced to express. The metabolic characteristics of BBR were analyzed in the CYP51 enzyme lysate system. The results showed that CYP51 in the gut microbiota could bind stably with BBR, and the addition of voriconazole (a specific inhibitor of CYP51) slowed down the metabolism of BBR, which prevented the production of the demethylated metabolites thalifendine and berberrubine. This study demonstrated that CYP51 promoted the demethylation of BBR and enhanced its intestinal absorption, providing a new method for studying the metabolic transformation mechanism of isoquinoline alkaloids in vivo., Graphical abstract Image 1, Highlights • The demethylation metabolism of natural drugs difficult to absorb through the gut microbiota was first reported. • Six different methods were presented to explain the metabolic mechanism of natural isoquinoline alkaloids. • The findings provided a new idea for studying the mechanism of drug metabolism of gut microbiota.

High-fat diet (HFD) could induce obese and microbial dysbiosis, the latter of which has great impact on host health. Dietary polysaccharides are well known to have a wide range of biological benefits for bowel health. In this study, we investigated the effects of rapeseed polysaccharide (RSP) on overweight and gut microbiota in high-fat-diet (HFD) fed rats. RSP effectively alleviated the hyperglycemia and lipid metabolic disorder in serum, which was found closely related to the modulation of intestinal microbiota. Supplementation of RSP regulated the intestinal microbiome by increasing the proportion of butyrate acid producer Blautia (P

It has been shown that whole grains and dietary fiber are important for their fermentation characteristics in the large intestine, drawing more and more attention to quinoa and quinoa polysaccharides. In this study, we evaluated the prebiotic effect of quinoa seeds and quinoa polysaccharides after human simulated digestion. The modulatory effect of the quinoa and quinoa polysaccharides (QPs) on the gut microbiota was evaluated by the in vitro fermentation using human fecal microbiota. The yield of polysaccharides extraction was 15.45%. The digestibility of the cooked and uncooked quinoa after simulation of human digestion was 69.04% and 64.09%, respectively. The effect on the microbiota composition and their metabolic products was determined by the assessment of pH, short‐chain fatty acids (SCFAs), and changes in the bacterial population. After 24 hr anaerobic incubation, the total SCFAs of cooked, uncooked quinoa, and quinoa polysaccharides were 82.99, 77.11, and 82.73 mM, respectively with a pH decrease. At the phylum, genus, and class level, it has been found that the quinoa substrates enhance the growth of certain beneficial bacteria such as Prevotella and Bacteroides. Quinoa polysaccharides can be considered prebiotic due to their ability to increase Bifidobacterium and Collinsella. Principal component analysis (PCA) showed that there was a distinct modulating effect on the fecal microbiota which represents different distribution. Our research suggests that quinoa and quinoa polysaccharides have a prebiotic potential due to their association with the positive shifts in microbiota composition and short‐chain fatty acids production, which highlights the importance of further studies around this topic., Quinoa and quinoa polysaccharides can modulate the gut microbiota. Quinoa and quinoa polysaccharides have a prebiotic effects.

BACKGROUND AND AIMS: Biliary atresia (BA) is a cholestatic, fibro-obliterative cholangiopathy of unknown etiology. BA is primarily treated by a surgical approach, i.e. the Kasai portoenterostomy (KPE), to obtain clearance of jaundice (COJ). The gut microbiota (GM) composition has been associated with the course of several cholestatic liver diseases. It is largely unknown, however, whether GM composition associates with the outcome of KPE. We compared the GM composition of BA patients and controls and assessed if GM composition before KPE was related to COJ after KPE.METHODS: We compared feces of term born BA patients before KPE and controls (patients undergoing inguinal hernia repair) by 16S rRNA sequencing. Composition and alpha diversity of the GM were compared between BA and controls before KPE and after KPE, between patients with COJ vs. without COJ (total serum bilirubin RESULTS: Alpha diversity was comparable between BA (n = 12, age 1.6[1.3-1.8]mo) and controls (n = 6, age 2.0[1.4-2.1]mo; P = 0.22). Compared to controls, BA patients had lower abundances of Bifidobacteriaceae (β=-1.98, P CONCLUSIONS: The gut microbiota of biliary atresia patients prior to Kasai portoenterostomy associates with outcome, clearance of jaundice, suggestive of predictive and mechanistic roles of the gut microbiota composition in bile homeostasis.

Background Existing evidence suggest that lactoferrin might be beneficial for Alzheimer's disease, while precise mechanisms are not fully elucidated. Objective To determine the effects of lactoferrin intervention on cognitive function from APPswe/PS1dE9 (APP/PS1) mice, and potential mechanisms involved. Design Both the young and middle-aged male APP/PS1 mice were divided into the control and lactoferrin intervention groups with 16 weeks' intervention. Results Lactoferrin had no effects on cognitive function for both the young and middle-aged mice, and no key markers involved in Aβ, tau pathology, neuro-inflammation and synaptic plasticity were altered after lactoferrin intervention. With regards to gut microbiota profiles, in the young APP/PS1 mice, lactoferrin elevated the α diversity index including ACE and Chao 1, and reduced the relative abundance of the genera Bacteroides and Alistipes and elevated Oscillibacter; in addition, Oscillibacter, Anaerotruncus, EF096579_g, EU454405_g, Mollicutes_RF39, EU474361_g, EU774448_g, and EF096976_g were specifically abundant via linear discriminant analysis with effect size (LEfSe) analysis. In the middle-aged APP/PS1 mice, the relative abundance of the phylum Proteobacteria, as well as the genera Oscillospira, Coprococcus, and Ruminococcus was significantly reduced post lactoferrin; additionally, S24_7, Bacteroidia, Bacteroidetes, and Methylobacterium were specific via LEfSe analysis in the lactoferrin group. Conclusions Dietary lactoferrin might be beneficial for gut microbiota homeostasis although it might have no effects on cognition.

Background Akkermansia muciniphila is a member of the human gut microbiota where it resides in the mucus layer and uses mucin as the sole carbon, nitrogen and energy source. A. muciniphila is the only representative of the Verrucomicrobia phylum in the human gut. However, A. muciniphila 16S rRNA gene sequences have also been found in the intestines of many vertebrates. Results We detected A. muciniphila-like bacteria in the intestines of animals belonging to 15 out of 16 mammalian orders. In addition, other species belonging to the Verrucomicrobia phylum were detected in fecal samples. We isolated 10 new A. muciniphila strains from the feces of chimpanzee, siamang, mouse, pig, reindeer, horse and elephant. The physiology and genome of these strains were highly similar in comparison to the type strain A. muciniphila MucT. Overall, the genomes of the new strains showed high average nucleotide identity (93.9 to 99.7%). In these genomes, we detected considerable conservation of at least 75 of the 78 mucin degradation genes that were previously detected in the genome of the type strain MucT. Conclusions The low genomic divergence observed in the new strains may indicate that A. muciniphila favors mucosal colonization independent of the differences in hosts. In addition, the conserved mucus degradation capability points towards a similar beneficial role of the new strains in regulating host metabolic health.

Background Through an arsenal of microbial enzymes, the gut microbiota considerably contributes to human metabolic processes, affecting nutrients, drugs, and environmental poisons. Azoreductases are a predominant group of microbiota-derived enzymes involved in xenobiotic metabolism and drug activation, but little is known about how compositional changes in the gut microbiota correlate with its azo-reducing activity. Results To this end, we used high-throughput 16S rRNA amplicon sequencing, with Illumina MiSeq, to determine the microbial community composition of stool samples from 16 adults with different azo-reducing activity. High azo-reducing activity positively correlated with the relative abundance of phylum Firmicutes (especially genera Streptococcus and Coprococcus) but negatively with phylum Bacteroidetes (especially genus Bacteroides). Typical variations in the Firmicutes-to-Bacteroidetes and Prevotella-to-Bacteroides ratios were observed among samples. Multivariate analysis of the relative abundance of key microbial taxa and other diversity parameters confirmed the Firmicutes proportion as a major variable differentiating high and non-azo-reducers, while Bacteroidetes relative abundance was correlated with azo-reduction, sex, and BMI. Conclusions This pilot study showed that stool samples with higher azo-reducing activity were enriched in Firmicutes but with relatively fewer Bacteroidetes. More samples and studies from different geographical areas are needed to bolster this conclusion. Better characterization of different azoreductase-producing gut microbes will increase our knowledge about the fate and differential human responses to azodye-containing drugs or orally consumed chemicals, thus contributing to efforts towards implementing microbiome testing in precision medicine and toxicology.

Vitamin D and its receptor are involved in health and diseases through multiple mechanisms including the immune system and gut microbiota modulations. Gut microbiota variations have huge implications in intestinal and extra-intestinal disorders such as colorectal cancer (CRC). This review highlights the preventive role of vitamin D in colorectal tumorigenesis through the effects on the immune system and gut microbiota modulation. The different associations between vitamin D, gut microbial homeostasis, immune system, and CRC, are dissected. Vitamin D is supposed to exert several chemopreventive effects on CRC including direct antineoplastic mechanisms, the effects on the immune system, and gut microbiota modulation. Large clinical studies with a randomized design, are required to confirm the role of vitamin D in CRC, confirming its key role in the complex interplay between the gut immune system and microbiota.