Characterisation of the faecal microbiota in Japanese patients with paediatric-onset primary sclerosing cholangitis

Iwasawa, Kentaro; Suda, Wataru; Tsunoda, Tomoyuki; Oikawa-Kawamoto, Manari; Umetsu, Shuichiro; Inui, Ayano; Fujisawa, Tomoo; Morita, Hidetoshi; Sogo, Tsuyoshi; Hattori, Masahira

doi:10.1136/gutjnl-2016-312533

Cited by 58 publications

(57 citation statements)

References 5 publications

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“…These results are consistent with the recent work of Kummen and colleagues who described a reduced bacterial diversity in PSC, regardless of the presence of IBD (5). In another study performed in a pediatric population of PSC and ulcerative colitis (UC) a lower species richness and abundance of Enterococcus (E. faecalis especially), Streptococcus (with prevalence of S. parasanguinis) and Veillonella species were found (6).…”

supporting

confidence: 92%

The “gut microbiota” hypothesis in primary sclerosing cholangitis

Pontecorvi¹,

Carbone²,

Invernizzi³

2016

Ann. Transl. Med.

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supporting

confidence: 92%

The “gut microbiota” hypothesis in primary sclerosing cholangitis

Pontecorvi¹,

Carbone²,

Invernizzi³

2016

Ann. Transl. Med.

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“…But in contrast to the study by Kummen et al [250], they could not find the difference in Veillonella between PSC patients and UC patients and insisted that the abundances of four taxa (Veillonella, Clostridiales, Lachnospiraceae and Coprococcus) was more useful for discriminating PSC from healthy subjects than the abundance of the genus Veillonella only [251]. Another letter to the editor by Iwasawa et al [252] reported increased Enterococcus, and decreased Parabacteroides in the feces of 27 Japanese children with PSC and IBD compared with age-matched healthy controls. The abundance of Faecalibacterium, Ruminococcus and Roseburia were higher in these patients than age-matched children with UC [252].…”

Section: Primary Sclerosing Cholangitis (Psc)mentioning

confidence: 87%

Role of Gut Dysbiosis in Liver Diseases: What Have We Learned So Far?

Fukui

2019

Diseases

106

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Accumulating evidence supports that gut dysbiosis may relate to various liver diseases. Alcoholics with high intestinal permeability had a decrease in the abundance of Ruminnococcus. Intestinal dysmotility, increased gastric pH, and altered immune responses in addition to environmental and genetic factors are likely to cause alcohol-associated gut microbial changes. Alcohol-induced dysbiosis may be associated with gut barrier dysfunction, as microbiota and their products modulate barrier function by affecting epithelial pro-inflammatory responses and mucosal repair functions. High levels of plasma endotoxin are detected in alcoholics, in moderate fatty liver to advanced cirrhosis. Decreased abundance of Faecalibacterium prausnitzii, an anti-inflammatory commensal, stimulating IL-10 secretion and inhibiting IL-12 and interferon-γ expression. Proteobacteria, Enterobacteriaceae, and Escherichia were reported to be increased in NAFLD (nonalcoholic fatty liver disease) patients. Increased abundance of fecal Escherichia to elevated blood alcohol levels in these patients and gut microbiota enriched in alcohol-producing bacteria produce more alcohol (alcohol hypothesis). Some undetermined pathological sequences related to gut dysbiosis may facilitate energy-producing and proinflammatory conditions for the progression of NAFLD. A shortage of autochthonous non-pathogenic bacteria and an overgrowth of potentially pathogenic bacteria are common findings in cirrhotic patients. The ratio of the amounts of beneficial autochthonous taxa (Lachnospiraceae + Ruminococaceae + Veillonellaceae + Clostridiales Incertae Sedis XIV) to those of potentially pathogenic taxa (Enterobacteriaceae + Bacteroidaceae) was low in those with early death and organ failure. Cirrhotic patients with decreased microbial diversity before liver transplantation were more likely to develop post-transplant infections and cognitive impairment related to residual dysbiosis. Patients with PSC had marked reduction of bacterial diversity. Enterococcus and Lactobacillus were increased in PSC patients (without liver cirrhosis.) Treatment-naive PBC patients were associated with altered composition and function of gut microbiota, as well as a lower level of diversity. As serum anti-gp210 antibody has been considered as an index of disease progression, relatively lower species richness and lower abundance of Faecalibacterium spp. in gp210-positive patients are interesting. The dysbiosis-induced altered bacterial metabolites such as a hepatocarcinogenesis promotor DCA, together with a leaky gut and bacterial translocation. Gut protective Akkermansia and butyrate-producing genera were decreased, while genera producing-lipopolysaccharide were increased in early hepatocellular carcinoma (HCC) patients.

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“…In contrast, patients with PSC have marked reductions in Clostridiales II , Prevotella and Roseburia , and Bacteroides , compared to patients with IBD alone and healthy controls . Actinobacteria, Proteobacteria, Streptococcus and Rothia have been reported to be overrepresented in patients with PSC compared with healthy controls and patients with inflammatory bowel disease . Mucosa‐associated bacteria as opposed to stool was also found with a lower bacterial diversity in patients with PSC, with an underrepresentation of an uncultured Clostriadiales II .…”

Section: Interplay Between the Gut Microbiota And Primary Sclerosing mentioning

confidence: 95%

Review article: the evidence that vancomycin is a therapeutic option for primary sclerosing cholangitis

Damman

Rodríguez

Ali

et al. 2018

Aliment Pharmacol Ther

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SummaryBackground and Aims: PSC is an autoimmune biliary inflammatory disorder that is often associated with inflammatory bowel disease (IBD), with 50%-75% of patients with PSC having coexisting IBD, most commonly ulcerative colitis. Currently, no medical therapies have been shown to improve the disease course or slow its progression. However, ongoing research has resulted in a growing interest in the use of antibiotics for treatment of PSC, of which vancomycin is the most studied. In this review, we summarise the current evidence on the use of vancomycin in PSC and comment on future research areas of interest.Methods: A comprehensive PUBMED and EMBASE literature search for articles on vancomycin, PSC, therapeutic options and microbiome was performed.Results: Two randomised clinical trials, three case series and two case reports were included in the study. These include uncontrolled data from at least 98 patients that include promising improvements in biochemistry and imaging. Optimal dosing regimens are unclear. Conclusion:Vancomycin is one of the most studied antibiotics used in the treatment of PSC with promising results. There is not currently sufficient evidence to support treatment recommendations. Further research is needed to establish if vancomycin is a PSC treatment.

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Characterisation of the faecal microbiota in Japanese patients with paediatric-onset primary sclerosing cholangitis

Cited by 58 publications

References 5 publications

The “gut microbiota” hypothesis in primary sclerosing cholangitis

The “gut microbiota” hypothesis in primary sclerosing cholangitis

Role of Gut Dysbiosis in Liver Diseases: What Have We Learned So Far?

Review article: the evidence that vancomycin is a therapeutic option for primary sclerosing cholangitis

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