DSS induced colitis increases portal LPS levels and enhances hepatic inflammation and fibrogenesis in experimental NASH

Gäbele, Erwin; Dostert, K; Hofmann, Claudia; Wiest, Reiner; Schölmerich, Jürgen; Hellerbrand, Claus; Obermeier, Florian

doi:10.1016/j.jhep.2011.02.035

Cited by 259 publications

(226 citation statements)

References 38 publications

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“…It is generally believed that the initial magnitude of the immune reaction determines the immunological fate, namely immune priming or immune tolerance (32). This 2-pronged phenomenon might account for the discrepancy between our findings and those from previous reports illustrating that continuous mild intestinal inflammation induced by chronic DSS administration enhanced hepatic inflammation and fibrogenesis in an experimental NASH model (33).…”

Section: Discussioncontrasting

confidence: 83%

Intestinal barrier regulates immune responses in the liver via IL-10–producing macrophages

Taniki¹,

Nakamoto²,

Chu³

et al. 2018

JCI Insight

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Section: Discussioncontrasting

confidence: 83%

Intestinal barrier regulates immune responses in the liver via IL-10–producing macrophages

Taniki¹,

Nakamoto²,

Chu³

et al. 2018

JCI Insight

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“…Of further interest is the study of Laroui et al, whose findings suggest that DSS is responsible for colitis development by forming "nanolipocomplexes" with MCFAs in the colon (27). Other studies have also shown that DSS treatment paired with HFD consumption produces a more aggressive form of colitis than DSS coupled with a LFD (17,29,40,41). The data from our study contradict the findings of Laroui et al, since we show, in two separate experiments, that the diets with the greatest content of SFAs, MCFAs in particular, result in the smallest tumor burden and lowest mortality rate.…”

Section: Discussionmentioning

confidence: 99%

High-fat diets rich in saturated fat protect against azoxymethane/dextran sulfate sodium-induced colon cancer

Enos

Velázquez

McClellan

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Hepatic TLR4 mRNA expression and plasma endotoxin levels were proved to be increased in NASH patients compared with NAFL patients [48]. Induction of an intestinal inflammation by dextran sulfate sodium in experimental NASH promotes LPS translocation, hepatic inflammation, and fibrogenesis [49]. Our group reported enhanced α-SMA expression (suggesting hepatic stellate cell activation), elevated liver LBP mRNA levels, increased intestinal permeability, and decreased intestinal TJP expression in the rat NASH model fed a choline-deficient L -amino-acid-defined diet [50].…”

Section: Nonalcoholic Fatty Liver Diseasesmentioning

confidence: 99%

Increased Intestinal Permeability and Decreased Barrier Function: Does It Really Influence the Risk of Inflammation?

2016

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Background: Increased intestinal permeability due to barrier dysfunction is supposed to cause microbial translocation which may induce low-grade inflammation in various diseases. However, this series of events has not been comprehensively evaluated yet. Summary: Intestinal epithelial barrier dysfunction and increased permeability have been described in patients with inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), alcoholic liver disease, nonalcoholic steatohepatitis (NASH), liver cirrhosis, acute pancreatitis, primary biliary cholangitis (PBC), type 1 and type 2 diabetes, chronic kidney disease, chronic heart failure (CHF), depression, and other diseases. Most clinical reports used either permeability assays of challenge tests or measurement of circulating bacterial markers like endotoxin for assessment of ‘the leaky gut'. The intestinal permeability assessed by the challenge tests has often been related to the changes of tight junction proteins in the epithelium or circulating endotoxin levels. In patients with IBD, alcoholic liver disease, NASH, liver cirrhosis, PBC, obstructive jaundice, severe acute pancreatitis, and CHF, endotoxemia and proinflammatory cytokinemia have been found in addition to increased permeability. In the serum of patients with IBS and depression, antiflagellin antibodies and antilipid A antibodies were detected, respectively, together with increased permeability and proinflammatory cytokinemia. The site of infection, which is localized to the intestine in IBD and IBS, includes various extraintestinal organs in other diseases. The relation of gut dysbiosis to intestinal barrier dysfunction has gradually been clarified. Key Messages: Although no direct cause-and-effect relationship has been confirmed, all clinical and experimental data suggest the importance of intestinal hyperpermeability in the inflammatory changes of various diseases. Increased intestinal permeability is a new target for disease prevention and therapy. Considering the close relationship of ‘the leaky gut' and gut dysbiosis to the major diseases, we can conclude that meticulous dietetic and probiotic approaches to recover healthy microbiota have the potential to make a breakthrough in the management of these diseases tomorrow.

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DSS induced colitis increases portal LPS levels and enhances hepatic inflammation and fibrogenesis in experimental NASH

Cited by 259 publications

References 38 publications

Intestinal barrier regulates immune responses in the liver via IL-10–producing macrophages

Intestinal barrier regulates immune responses in the liver via IL-10–producing macrophages

High-fat diets rich in saturated fat protect against azoxymethane/dextran sulfate sodium-induced colon cancer

Increased Intestinal Permeability and Decreased Barrier Function: Does It Really Influence the Risk of Inflammation?

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