Intestinally derived bacterial products stimulate development of nonalcoholic steatohepatitis

Abstract : Fatty livers are susceptible to factors that cause inflammation and fibrosis, but fat deposition and the inflammatory response can be dissociated. While nonalcoholic fatty liver disease (NAFLD), caused by pathologic fat accumulation inside the liver, can remain stable for several years, in other cases NAFLD progresses to nonalcoholic steatohepatitis (NASH), which is characterized by fat accumulation and inflammation and is not a benign condition. In this review, we discuss the NASH host cells and microbial mechanisms that stimulate inflammation and predispose the liver to hepatocyte injury and fibrotic stages via increased lipid deposition. We highlight the interactions between intestine-derived bacterial products, such as lipopolysaccharide, and nutritional models of NAFLD and/or obese individuals. The results of modulating enteric microbiota suggest that gut-derived endotoxins may be essential determinants of fibrotic progression and regression in NASH.
Complete list of metadatas

Cited literature [121 references]  Display  Hide  Download

https://hal-univ-rennes1.archives-ouvertes.fr/hal-02020468
Contributor : Laurent Jonchère <>
Submitted on : Thursday, April 4, 2019 - 10:58:41 AM
Last modification on : Thursday, June 27, 2019 - 1:14:43 PM
Long-term archiving on : Friday, July 5, 2019 - 1:08:12 PM

File

Dornas et al_2019_Intestinally...
Files produced by the author(s)

Identifiers

Citation

Waleska Dornas, Vincent Lagente. Intestinally derived bacterial products stimulate development of nonalcoholic steatohepatitis. Pharmacological Research, Elsevier, 2019, 141, pp.418-428. ⟨10.1016/j.phrs.2019.01.026⟩. ⟨hal-02020468⟩

Share

Metrics

Record views

66

Files downloads

40