There were alterations of gut microbiota in IBS patients, and it implied that alterations of gut microbiota might be involved in the pathogenesis of IBS. However, the species-specific alterations of gut microbiota were different between IBS patients from China and other regions.
Altered gut microbiota are assumed to be involved in the pathogenesis of irritable bowel syndrome (IBS). However, gut microbiota alterations reported in different studies are divergent and sometimes even contradictory. To better elucidate the relationship between altered gut microbiota and IBS, we characterized fecal microbiota of diarrhea-predominant IBS (IBS-D) patients and further explored the effect of rifaximin on gut microbiota using bacterial 16S rRNA gene-targeted pyrosequencing. In our study, IBS-D patients defined by Rome III criteria and age-and-gender matched healthy controls (HC) were enrolled to investigate the fecal microbiota alterations. These IBS-D patients were then treated with rifaximin for 2 weeks and followed up for 10 weeks. Fecal microbiota alterations, small intestine bacterial overgrowth (SIBO) and gastrointestinal (GI) symptoms of IBS-D patients were analyzed before and after treatment. Our results showed fecal microbiota richness but not diversity was decreased in IBS-D patients as compared to HC and there were alterations of fecal microbiota at different taxonomy levels. The abundant phyla Firmicutes was significantly decreased and Bacteroidetes was increased in IBS-D patients. Moreover, the alterations of predominant fermenting bacteria such as Bacteroidales and Clostridiales might be involved in the pathophysiology of IBS-D. In addition, rifaximin was effective in terms of SIBO eradication and even GI symptoms of IBS-D patients achieved at least 10-week improvement after treatment. Furthermore, rifaximin induced alterations of some special bacteria rather than affected the overall composition of microbiota in IBS-D patients. Meanwhile, a potential decrease in propanoate and butanoate metabolism was found in these IBS-D patients after rifaximin treatment. Taken together, there were alterations of gut microbiota in IBS-D patients as compared to HC. Rifaximin could relieve GI symptoms, modify gut microbiota in IBS-D patients and eradicate SIBO in those patients with SIBO, suggesting an additional therapeutic mechanism of rifaximin in the treatment of IBS-D. Our findings of compositional gut microbiota alterations in IBS-D and the effect of rifaximin on the gut microbiota implied that altered gut microbiota were associated with the pathogenesis of IBS.
Summary Background While the incidence of inflammatory bowel disease (IBD) has stabilised in the West, it is still increasing in several newly industrialised countries. Aims To investigate whether the environmental and dietary risk factors for IBD differ between Eastern and Western populations Methods We systematically searched PubMed, Embase, and Web of Science for studies published from inception through June 30, 2020. Data were pooled using a random effects model. Results Overall, 255 studies were assessed. We identified 25 risk factors for IBD, seven of which were noted in both Eastern and Western populations: family history of Crohn's disease [CD] or ulcerative colitis [UC], former smoking (CD/UC), smoking (CD), appendicectomy (CD), tonsillectomy (CD), meat and meat products (CD), and vitamin D deficiency (UC). The remaining factors, including urban living, current smoking, antibiotics, oral contraceptives, caesarean section, isotretinoin, total energy, fat, cholesterol, fatty acids and their sub‐classifications, eggs, and soft drinks, were associated with an increased risk of IBD in Western or Eastern populations only. We identified 21 protective factors for IBD, among which eight were common in the East and West: farm animals (CD/UC), Helicobacter pylori infection (CD/UC), multiple births (CD), physical activity (CD), history of breastfeeding (CD), pets (UC), current smoking (UC), and coffee intake (UC). Ten factors conferred protection against IBD in Western populations only, whereas eight factors conferred protection against IBD in Eastern populations only. Conclusions Numerous environmental and dietary factors influenced the development of IBD in both Western and Eastern populations, whereas certain factors influenced IBD risk differently in these populations.
Background Alterations in gut microbiota and short-chain fatty acids (SCFAs) have been reported in inflammatory bowel disease (IBD), but the results are conflicting. The aim of this study was to perform a meta-analysis to explore the characterization of SCFAs in IBD patients and their potential role in the occurrence and development of IBD. Methods Case–control studies investigating SCFAs in IBD patients were identified from several English databases. The standardized mean difference (SMD) with 95% confidence interval (CI) was calculated using the random-effects model. Results The SMDs of acetate, valerate, and total SCFAs in ulcerative colitis (UC) patients were –0.51 (95% CI, –0.90 to –0.13), –0.65 (95% CI, –1.02 to –0.28), and –0.51 (95% CI, –0.95 to –0.07), respectively. The SMDs of acetate, propionate, and butyrate in patients with active UC were –1.74 (95% CI, –3.15 to –0.33), –2.42 (95% CI, –4.24 to –0.60), and –1.99 (95% CI, –3.39 to –0.60), respectively. However, the SMD of butyrate in UC patients in remission was 0.72 (95% CI, 0.34 to 1.11). In addition, the SMDs of acetate, butyrate, and valerate in Crohn’s disease (CD) patients were –1.43 (95% CI, –2.81 to –0.04), –0.77 (95% CI, –1.39 to –0.14), and –0.75 (95% CI, –1.47 to –0.02), respectively. Finally, the SMDs of acetate, propionate, butyrate, valerate, and lactate in IBD patients were –2.19 (95% CI, –3.98 to –0.39), –1.64 (95% CI, –3.02 to –0.25), –1.98 (95% CI, –3.93 to –0.03), –0.55 (95% CI, –0.93 to –0.18), and 4.02 (95% CI, 1.44 to 6.61), respectively. Conclusions There were alterations of SCFAs in IBD patients, and inconsistent SCFA alterations were found in CD and UC. More importantly, inverse SCFA alterations existed in patients with active UC and those in remission.
Highlights d Injury increases peroxisomes in Drosophila and human gastrointestinal stem cells d Peroxisomes are essential for intestinal stem cell differentiation in Drosophila d Peroxisomes modulate RAB7-mediated late endosome maturation d Promoted peroxisome proliferation accelerates intestinal epithelial repair
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