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Cancer is one of the leading global causes of death in both men and women. Colorectal cancer (CRC) alone accounts for ∼10 % of total new global cases and poses an over 4% lifetime risk of developing cancer. Recent advancements in the field of biotechnology and microbiology concocted novel microbe-based therapies to treat various cancers, including CRC. Microbes have been explored for human use since centuries, especially for the treatment of various ailments. The utility of microbes in cancer therapeutics is widely explored, and various bacteria, fungi, and viruses are currently in use for the development of cancer therapeutics. The human gut hosts about 100 trillion microbes that release their metabolites in active, inactive, or dead conditions. Microbial secondary metabolites, proteins, immunotoxins, and enzymes are used to target cancer cells to induce cell cycle arrest, apoptosis, and death. Various approaches, such as dietary interventions, the use of prebiotics and probiotics, and fecal microbiota transplantation have been used to modulate the gut microbiota in order to prevent or treat CRC pathogenesis. The present review highlights the role of the gut microbiota in CRC precipitation, the potential mechanisms and use of microorganisms as CRC biomarkers, and strategies to modulate microbiota for the prevention and treatment of CRC. [ABSTRACT FROM AUTHOR]

Children with short bowel syndrome (SBS) frequently struggle with malabsorption and poor growth. The intestinal microbiota plays an important role in gut function, and children with SBS have known deficiencies in some commensal gut microbes. One strategy to enhance the gut microbiota is by taking probiotics. However, the efficacy of this approach is not well established. We hypothesized that probiotic supplementation would result in increased levels of the supplemented bacteria and improved growth. Children with SBS who had weaned from parenteral nutrition but with suboptimal growth were randomized to receive probiotics (Lactobacillus rhamnosus and Lactobacillus johnsonii) or placebo daily for 2 mo. The gut microbiota from monthly stool samples were compared between groups using 16S ribosomal ribonucleic acid sequencing and quantitative polymerase chain reaction. Growth between groups was also compared. Statistical analysis was completed using Mann-Whitney, Kruskal-Wallis, and chi-square tests as appropriate. Eighteen children with SBS completed the study (n = 9 per group). There were no significant changes to the major bacterial families in either group. Median relative abundance of Lactobacillus did not differ between groups at baseline or at the end of the study (7.67 versus 13.23, P = 0.523 and 1.93 versus 15.8, P = 0.161). Median z scores for weight and length did not differ between groups at the beginning or end of the study. The efficacy of daily probiotic use in children with intestinal failure is unknown. In this study, Lactobacillus probiotics did not result in a predictable change to the fecal microbiota or overall growth compared with placebo in these patients. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by progressive polyarthritis that leads to cartilage and bone damage. Pre-clinical RA is a prolonged state before clinical arthritis and RA develop, in which autoantibodies (antibodies against citrullinated proteins, rheumatoid factors) can be present due to the breakdown of immunologic self-tolerance. As early treatment initiation before the onset of polyarthritis may achieve sustained remission, optimize clinical outcomes, and even prevent RA progression, the pre-clinical RA stage is showing the prospect to be the window of opportunity for RA treatment. Growing evidence has shown the role of the gut microbiota in inducing systemic inflammation and polyarthritis via multiple mechanisms, which may involve molecular mimicry, impaired intestinal barrier function, gut microbiota-derived metabolites mediated immune regulation, modulation of the gut microbiota's effect on immune cells, intestinal epithelial cells autophagy, and the interaction between the microbiome and human leukocyte antigen alleles as well as microRNAs. Since gut microbiota alterations in pre-clinical RA have been reported, potential therapies for modifying the gut microbiota in pre-clinical RA, including natural products, antibiotic therapy, fecal microbiota transplantation, probiotics, microRNAs therapy, vitamin D supplementation, autophagy inducer-based treatment, prebiotics, and diet, holds great promise for the successful treatment and even prevention of RA via altering ongoing inflammation. In this review, we summarized current studies that include pathogenesis of gut microbiota in RA progression and promising therapeutic strategies to provide novel ideas for the management of pre-clinical RA and possibly preventing arthritis progression. • Pre-clinical RA stage is the window of opportunity in RA treatment. • Gut microbiota alteration may promote immune system dysfunction and joint damage. • Balancing gut microbiota may restore immune system dysfunction. • Combination therapy target on microbiota need to be developed. • Microbiota based intervention is promising in prevent RA development. [ABSTRACT FROM AUTHOR]

Cachexia is a common pathological condition in cancer patients, affecting prognosis and treatment outcomes. The relationship between cachexia and gut microbiota and short-chain fatty acids (SCFAs) remains understudied. This research aimed to establish a cachexia mouse model and explore the gut microbiota-SCFAs connection. The study provides fundamental insights into the regulatory mechanisms of cancer cachexia and potential therapeutic strategies. A cachexia mouse model was created using C26 cells, with relevant indicators measured. Histological and immunohistochemical analyses assessed muscle structure and protein expression. ELISA was performed to detect the levels of IL-1β, IL-6, TNF-α, and LPS in serum to evaluate inflammation.16S rDNA sequencing and GC-MS quantified gut microbiota and SCFAs. Bioinformatics analysis identified indicator species and explored microbiota-SCFAs correlations.ROC analysis was performed to assess the potential of gut microbiota and SCFAs in identifying cachexia. The cachexia mouse model exhibited weight loss, muscle atrophy, and elevated inflammatory factors. Gut microbiota in cachexia mice showed decreased diversity and imbalance. Fourteen bacterial genera were identified as potential cachexia indicators. Functional prediction indicated alterations in the functional composition of gut microbial communities in cachexia mice, particularly in carbohydrate and lipid metabolism pathways. Four SCFAs showed significant changes, potentially serving as diagnostic factors. Specific microbial taxa were positively or negatively correlated with changes in SCFAs, and these microbial taxa and differential SCFAs were also correlated with inflammatory cytokines. Our study uncovers the gut microbiota and SCFAs features in a cachexia mouse model, revealing novel correlations between them. These newfound insights into the interplay between cachexia, gut microbiota, and SCFAs provide a crucial foundation for understanding the mechanisms behind cancer cachexia development and potential therapeutic approaches. • Diminished and disrupted gut microbial diversity observed in cachectic mice, accompanied by alterations in the functional composition of gut microbial communities. • Disturbed levels of SCFAs detected in the fecal samples of cachectic mice. • Potential utilization of intestinal microbiota and SCFAs as discerning markers for assessing cachexia in mice. • There is a potential correlation among the gut microbiota composition, SCFAs, and inflammatory factors in cachexic mice. [ABSTRACT FROM AUTHOR]

Age-related macular degeneration (AMD) is a complex disease with increasing numbers of individuals being afflicted and treatment modalities limited. There are strong interactions between diet, age, the metabolome, and gut microbiota, and all of these have roles in the pathogenesis of AMD. Communication axes exist between the gut microbiota and the eye, therefore, knowing how the microbiota influences the host metabolism during aging could guide a better understanding of AMD pathogenesis. While considerable experimental evidence exists for a diet-gut–eye axis from murine models of human ocular diseases, human diet-microbiome-metabolome studies are needed to elucidate changes in the gut microbiome at the taxonomic and functional levels that are functionally related to ocular pathology. Such studies will reveal new ways to diminish risk for progression of- or incidence of- AMD. Current data suggest that consuming diets rich in dark fish, fruits, vegetables, and low in glycemic index are most retina-healthful during aging. • The etiology of AMD is multifactorial including nutritional factors, genetic variants mainly in the complement pathway, environmental risk factors, and the intestinal microbiome. • Nutritional risks for AMD are as great as the risk imposed by smoking. • Defining interactions between nutrition, metabolomes, microbiomes, physiological responses, and clinical ophthalmologic data represent an "interactome" network that may help identify novel biomarkers of AMD progression. • Clinical studies using plasma metabolites (lipids, advanced glycation end products, lutein, markers of barrier dysfunction) and inflammatory molecules will help elucidate interactions between the gut microbiome and AMD. [ABSTRACT FROM AUTHOR]

The human intestinal microbiota coevolves with its host through a symbiotic relationship and exerts great influence on substantial functions including aspects of physiology, metabolism, nutrition and regulation of immune responses leading to physiological homeostasis. Over the last years, several studies have been conducted toward the assessment of the host–gut microbiota interaction, aiming to elucidate the mechanisms underlying the pathogenesis of several diseases. A defect on the microbiota–host crosstalk and the concomitant dysregulation of immune responses combined with genetic and environmental factors have been implicated in the pathogenesis of inflammatory bowel diseases (IBD). To this end, novel therapeutic options based on the gut microbiota modulation have been an area of extensive research interest. In this review we present the recent findings on the association of dysbiosis with IBD pathogenesis, we focus on the role of gut microbiota on the treatment of IBD and discuss the novel and currently available therapeutic strategies in manipulating the composition and function of gut microbiota in IBD patients. Applicable and emerging microbiota treatment modalities, such as the use of antibiotics, prebiotics, probiotics, postbiotics, synbiotics and fecal microbiota transplantation (FMT) constitute promising therapeutic options. However, the therapeutic potential of the aforementioned approaches is a topic of investigation and further studies are needed to elucidate their position in the present treatment algorithms of IBD. • Microbes are key players for maintaining the homeostasis of immune system. • Gut microbiota imbalance and immunity defects have been implicated in gut inflammation. • Novel therapeutic advances for IBD management involve gut microbiota regulation. • Fecal microbiota transplantation is very promising for ulcerative colitis' treatment. [ABSTRACT FROM AUTHOR]