P871 Successful detection of dysbiosis and altered short-chain-fatty acids levels in in vitro colonic microbiota culture system using faecal samples of ulcerative colitis
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Ulcerative colitis (UC) involves chronic and recurring inflammation of the intestinal tract. It is widely recognised that the composition of gut microbiota and intestinal metabolites are altered in UC patients. There is increasing number of clinical studies which supports the idea that imbalance of gut microbiota (dysbiosis) plays a role in pathogenesis and/or progression of UC. We previously reported single–batch fermentation system (Takagi et al., PLoS One, 2016) which can approximately recapitulate the microbiota of fecal sample in vitro, and could detect the change of microbiota and metabolites when prebiotics were supplemented to the system. It prompted us to test if this system could actually detect the unbalanced fecal microbiota and metabolites of UC patients; which may suggest the potential usefulness of this system for preclinical evaluation of effect of probiotics and prebiotics before administration to patients. Fecal samples were obtained from 11 UC patients and 13 healthy human subjects (HS). Fecal samples were applied to the single–batch fermentation system and aliquots of fermentation cultures were sampled to analyse the composition of bacteria and short-chain-fatty acids (SCFAs) concentration. Bacterial 16S rRNA gene sequencing was performed with Illumina MiSeq. Concentrations of SCFAs were measured using a high-performance liquid chromatograph. Bacterial component and SCFAs concentration were compared between UC and HS. The bacterial diversity and richness in fecal samples were maintained in corresponding fermentation cultures of both UC and HS. Comparison of principal coordinate plots of the unweighted UniFrac distance showed that compositional difference of microbiota between HS and UC patients were successfully reproduced in the single–batch fermentation system as observed in faces. Relative abundance of family Lachnospiraceae, which includes butyrate producing species, was significantly decreased in the microbiota of UC patients compared with those of HS, which was the same tendency as observed in faces. Butyrate generation was significantly decreased in the colon culture models of UC patients compared with those of HS and strongly correlated with relative abundance of family Lachnospiraceae. In this study, our new culture system could successfully recapitulate the previously shown dysbiosis of reduced family Lachnospiraceae and reduced butyrate level in UC patients in vitro. It may have a potential to be used as an in vitro evaluation system to check the intestinal environment in health and disease. It could be a good model to test whether dysbiosis can be corrected into symbiosis by adding prebiotics and/or probiotics to modify the gut microbiota community in each UC patient.Keywords:
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The gut microbiome has been shown to play a critical role in maintaining a healthy state. Dysbiosis of the gut microbiome is involved in modulating disease severity and potentially contributes to long-term outcomes in adults with COVID-19. Due to children having a significantly lower risk of severe illness and limited sample availability, much less is known about the role of the gut microbiome in children with COVID-19. It is well recognized that the developing gut microbiome of children differs from that of adults, but it is unclear if this difference contributes to the different clinical presentations and complications. In this review, we discuss the current knowledge of the gut microbiome in children with COVID-19, with gut microbiome dysbiosis being found in pediatric COVID-19 but specific taxa change often differing from those described in adults. Additionally, we discuss possible mechanisms of how the gut microbiome may mediate the presentation and complications of COVID-19 in children and the potential role for microbial therapeutics.
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The application of high-throughput sequencing technologies has greatly enhanced our understanding to the human microbiome. The causal relations between human microbiome and diseases have become a critical issue to elucidate disease development and develop precision medicine. Recently, the study about vaginal microbiome (the microbial flora that inhabits the female vagina) has received wide interests. It has been shown that dysbiosis of vaginal microbiome was closely related to the development of genital tract diseases. This article summarizes the interaction between vaginal microbiome and disease and the treatment for the dysbiosis of vaginal microbiome. The culturomics of virginal microbiome, engineered probiotics and synthetic microbiome were also proposed.
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It is well known that there is an imbalance of gut microbiota in liver diseases, our previous study has proved that Aronia melanocarpa polyphenols (AMPs) can modulate the gut microbiota and affect the progression of liver diseases. Here, we analyzed the gut microbiota by 16S rRNA sequencing and bioinformatic analysis to explored the changes of gut microbiota composition and functions after LPS and AMPs intervention. Our results showed that there were significant differences in the gut microbiota structure between different treatment groups, such as increasing the abundance of Lactobacillaceae and Muribaculaceae, decreasing the abundance of Ruminococcaceae and Acidaminococcaceae. Furthermore, PICRUSt prediction showed that 29 functional pathways have changed significantly which may promote the treatment of liver diseases. This study could help to supplement the information about the community of gut microbiota in liver diseases and provide a new strategy for the treatment of liver diseases.
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Diversity and activity of gut microbiota residing in humans and animals are significantly influenced by the diet. A quercetin containing diet is effective in recovering gut microbiota in mice after antibiotic treatment and may act as a prebiotic in combating gut dysbiosis.
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Previous studies suggested a possible gut microbiota dysbiosis in chronic heart failure (CHF). However, direct evidence was lacking. In this study, we investigated the composition and metabolic patterns of gut microbiota in CHF patients to provide direct evidence and comprehensive understanding of gut microbiota dysbiosis in CHF. We enrolled 53 CHF patients and 41 controls. Metagenomic analyses of faecal samples and metabolomic analyses of faecal and plasma samples were then performed. We found that the composition of gut microbiota in CHF was significantly different from controls. Faecalibacterium prausnitzii decrease and Ruminococcus gnavus increase were the essential characteristics in CHF patients' gut microbiota. We also observed an imbalance of gut microbes involved in the metabolism of protective metabolites such as butyrate and harmful metabolites such as trimethylamine N-oxide in CHF patients. Metabolic features of both faecal and plasma samples from CHF patients also significantly changed. Moreover, alterations in faecal and plasma metabolic patterns correlated with gut microbiota dysbiosis in CHF. Taken together, we found that CHF was associated with distinct gut microbiota dysbiosis and pinpointed the specific core bacteria imbalance in CHF, along with correlations between changes in certain metabolites and gut microbes.
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ENWEndNote BIBJabRef, Mendeley RISPapers, Reference Manager, RefWorks, Zotero AMA Frej-MÄ drzak M, Jeziorek M, Sarowska J, Jama-Kmiecik A, Choroszy-Król I. The role of probiotics and prebiotics in the proper functioning of gut microbiota and the treatment of diseases caused by gut microbiota dysbiosis. Nutrition, Obesity & Metabolic Surgery. 2020;7(1):9-15. doi:10.5114/noms.2020.94667. APA Frej-MÄ drzak, M., Jeziorek, M., Sarowska, J., Jama-Kmiecik, A., & Choroszy-Król, I. (2020). The role of probiotics and prebiotics in the proper functioning of gut microbiota and the treatment of diseases caused by gut microbiota dysbiosis. Nutrition, Obesity & Metabolic Surgery, 7(1), 9-15. https://doi.org/10.5114/noms.2020.94667 Chicago Frej-MÄ drzak, Magdalena, MaÅgorzata Jeziorek, Jolanta Sarowska, Agnieszka Jama-Kmiecik, and Irena Choroszy-Król. 2020. "The role of probiotics and prebiotics in the proper functioning of gut microbiota and the treatment of diseases caused by gut microbiota dysbiosis". Nutrition, Obesity & Metabolic Surgery 7 (1): 9-15. doi:10.5114/noms.2020.94667. Harvard Frej-MÄ drzak, M., Jeziorek, M., Sarowska, J., Jama-Kmiecik, A., and Choroszy-Król, I. (2020). The role of probiotics and prebiotics in the proper functioning of gut microbiota and the treatment of diseases caused by gut microbiota dysbiosis. Nutrition, Obesity & Metabolic Surgery, 7(1), pp.9-15. https://doi.org/10.5114/noms.2020.94667 MLA Frej-MÄ drzak, Magdalena et al. "The role of probiotics and prebiotics in the proper functioning of gut microbiota and the treatment of diseases caused by gut microbiota dysbiosis." Nutrition, Obesity & Metabolic Surgery, vol. 7, no. 1, 2020, pp. 9-15. doi:10.5114/noms.2020.94667. Vancouver Frej-MÄ drzak M, Jeziorek M, Sarowska J, Jama-Kmiecik A, Choroszy-Król I. The role of probiotics and prebiotics in the proper functioning of gut microbiota and the treatment of diseases caused by gut microbiota dysbiosis. Nutrition, Obesity & Metabolic Surgery. 2020;7(1):9-15. doi:10.5114/noms.2020.94667.
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Alcoholic liver disease (ALD) is a major health issue globally due to the consumption of alcoholic beverages. Thymus quinquecostatus Celak is a food additive and an edible herb that is widely used in Asia and possesses hepatoprotective activity, but the underlying mechanisms behind this protective activity are not completely understood. The purpose of this study was to investigate the hepatoprotective effects of Thymus quinquecostatus Celak extract (TQE) against ALD as well as the underlying mechanism based on gut microbiota and the gut-liver axis. TQE supplementation markedly alleviated chronic alcohol-induced liver injury in C57 mice. TQE also ameliorated gut barrier dysfunction induced by alcohol. Consequently, the activation of the lipopolysaccharide (LPS) translocation-mediated TLR4 pathway and the subsequent inflammatory response and ROS overproduction in the liver were suppressed. Meanwhile, alcohol-induced gut microbiota dysbiosis was also corrected by TQE. To further investigate the contribution of gut dysbiosis correction to the beneficial effects of TQE on ALD, a fecal microbiota transplantation study was conducted. TQE-manipulated gut microbiota transplantation markedly counteracted the alcohol-induced gut dysbiosis in the recipient mice. In parallel with gut dysbiosis correction, liver damage was partly ameliorated in the recipient mice. Gut barrier dysfunction, endotoxemia, TLR4 pathway induction as well as downstream inflammatory response and ROS overproduction were also partly suppressed due to gut dysbiosis correction in alcohol-fed recipient mice. In summary, these results suggest that gut dysbiosis correction contributes to the hepatoprotective effects of TQE against alcohol through the gut-liver axis.
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Gastrointestinal dysfunction is a common peripheral organ complication after traumatic brain injury (TBI), yet the underlying mechanism remains unknown. TBI has been demonstrated to cause gut microbiota dysbiosis in animal models, although the impacts of gut microbiota dysbiosis on gastrointestinal dysfunction were not examined. Bile acids are key metabolites between gut microbiota and host interactions. Therefore, the aim of this study was to investigate the mechanistic links between them by detecting the alterations of gut microbiota and bile acid profile after TBI. For that, we established TBI in mice using a lateral fluid percussion injury model. Gut microbiota was examined by 16S rRNA sequencing, and bile acids were profiled by ultra-performance liquid chromatography-tandem mass spectrometry. Our results showed that TBI caused intestinal inflammation and gut barrier impairment. Alterations of gut microbiota and bile acid profile were observed. The diversity of gut microbiota experienced a time dependent change from 1 h to 7 days post-injury. Levels of bile acids in feces and plasma were decreased after TBI, and the decrease was more significant in secondary bile acids, which may contribute to intestinal inflammation. Specific bacterial taxa such as Staphylococcus and Lachnospiraceae that may contribute to the bile acid metabolic changes were identifed. In conclusion, our study suggested that TBI-induced gut microbiota dysbiosis may contribute to gastrointestinal dysfunction via altering bile acid profile. Gut microbiota may be a potential treatment target for TBI-induced gastrointestinal dysfunction.
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