Response to ‘Faecal microbiota profiles as diagnostic biomarkers in primary sclerosing cholangitis’ by Rühlemann<i>et al</i>

Kummen, Martin; Hov, Johannes R.

doi:10.1136/gutjnl-2016-312347

Cited by 6 publications

(7 citation statements)

References 4 publications

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“…In a letter to the editor, Rühlemann et al [251] also admitted the enriched Veillonella in their 73 northern German patients with PSC compared with healthy controls. 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.…”

Section: Primary Sclerosing Cholangitis (Psc)contrasting

confidence: 65%

“…Bajer et al [249] found fecal Rothia, Enterococcus, Streptococcus, Clostridium, Veillonella and Haemophilus were increased in 43 Czech patients with PSC regardless of concomitant IBD compared with healthy subjects. Kummen et al [240] stressed that Veillonella genus in the feces showed a marked increase in 85 Norwegean PSC patients compared with both healthy controls and UC patients and thought it could potentially influence disease progression [250]. In a letter to the editor, Rühlemann et al [251] also admitted the enriched Veillonella in their 73 northern German patients with PSC compared with healthy controls.…”

Section: Primary Sclerosing Cholangitis (Psc)mentioning

confidence: 99%

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

Fukui

2019

Diseases

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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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Section: Primary Sclerosing Cholangitis (Psc)contrasting

confidence: 65%

Section: Primary Sclerosing Cholangitis (Psc)mentioning

confidence: 99%

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

Fukui

2019

Diseases

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“…Microbial components, their metabolites, or even microorganisms can disseminate systemically when the intestinal barrier is disrupted (as is the case with ''leaky gut'') (Kamada et al, 2013). Therefore, dissemination of gutderived microbial factors can contribute to the development and progression of diseases in extra-intestinal organs, including liver diseases such as alcohol-induced liver disease (Betrapally et al, 2016;Mutlu et al, 2012), non-alcoholic steatohepatitis (Boursier et al, 2016;Zhu et al, 2013), and primary sclerosing cholangitis (Kummen and Hov, 2016;Sabino et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Commensal Lactobacillus Controls Immune Tolerance during Acute Liver Injury in Mice

et al. 2017

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Gut-derived microbial antigens trigger the innate immune system during acute liver injury. During recovery, regulatory immunity plays a role in suppressing inflammation; however, the precise mechanism underlying this process remains obscure. Here, we find that recruitment of immune-regulatory classical dendritic cells (cDCs) is crucial for liver tolerance in concanavalin A-induced acute liver injury. Acute liver injury resulted in enrichment of commensal Lactobacillus in the gut. Notably, Lactobacillus activated IL-22 production by gut innate lymphoid cells and raised systemic IL-22 levels. Gut-derived IL-22 enhanced mucosal barrier function and promoted the recruitment of regulatory cDCs to the liver. These cDCs produced IL-10 and TGF-β through TLR9 activation, preventing further liver inflammation. Collectively, our results indicate that beneficial gut microbes influence tolerogenic immune responses in the liver. Therefore, modulation of the gut microbiota might be a potential option to regulate liver tolerance.

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“…Evidence from animal models [11] and success of antibiotic treatment in PSC patients [12] suggest that disruption of gut microbiota may play a significant role in pathogenesis of PSC. Recently, several studies described specific changes in the gut microbiota of PSC patients that were not related to dysbiosis with concomitant IBD [13][14][15][16][17][18][19][20] . However, those studies differed in sampling, experimental methods and design, in addition to outcome.…”

Section: Introductionmentioning

confidence: 99%