1998
DOI: 10.1111/j.1749-6632.1998.tb09016.x
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Effect of Bile Acids on Endotoxin in Vitro and in Vivo (Physico-Chemical Defense): Bile Deficiency and Endotoxin Translocation

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Cited by 21 publications
(19 citation statements)
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“…LPS and proinflammatory cytokines such as TNF-a and IFN-c are shown to induce TJP disruption through alterations to the apical junctional complex [30]. UDCA reportedly fragments endotoxin into smaller, non-toxic fragments [31] and inactivates endotoxin through its detergent activity [7]. Consistent with our study, treatment with UDCA has shown to suppress inflammatory response in an inflammation-mediated model of liver fibrosis induced by schistosomiasis [32].…”
Section: Discussionsupporting
confidence: 86%
See 1 more Smart Citation
“…LPS and proinflammatory cytokines such as TNF-a and IFN-c are shown to induce TJP disruption through alterations to the apical junctional complex [30]. UDCA reportedly fragments endotoxin into smaller, non-toxic fragments [31] and inactivates endotoxin through its detergent activity [7]. Consistent with our study, treatment with UDCA has shown to suppress inflammatory response in an inflammation-mediated model of liver fibrosis induced by schistosomiasis [32].…”
Section: Discussionsupporting
confidence: 86%
“…Recent studies have demonstrated a close association between the development of NASH and the activation of lipopolysaccharide (LPS)-induced Toll-like receptor 4 (TLR4) [6]. Furthermore, UDCA therapy is shown to counteract endotoxemia through reduced intestinal absorption and detoxification of LPS [7]. However, the exact mechanism underlying the beneficial effect of UDCA in NASH is yet to be fully elucidated.…”
Section: Introductionmentioning
confidence: 98%
“…1998). Bile acids can detoxify endotoxin (Bertok 1998), but it is not known if these acids can detoxify all of the endotoxin that originate from the rumen. High grain feeding can result in SARA and increase the starch content in the large intestine.…”
mentioning
confidence: 99%
“…Bile acid-induced liver injury may progress to cirrhosis and be complicated by endotoxemia and sepsis, because of a reduction in intestinal bile acids that have an important defensive role, fragmenting bacterial lipopolysaccharide (LPS) and enteroendotoxin to reduce intestinal absorption of these molecules (9,10). During the body's acute-phase response to injury or infection, extensive changes in plasma lipoproteins occur, including an increase in production and a decrease in catabolism of circulating lipoproteins (11).…”
mentioning
confidence: 99%