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Review
. 2014 Dec;3(6):377-85.
doi: 10.3978/j.issn.2304-3881.2014.12.04.

Innate immune signaling and gut-liver interactions in non-alcoholic fatty liver disease

Veerle Bieghs  1 , Christian Trautwein  1
Affiliations
Review

Innate immune signaling and gut-liver interactions in non-alcoholic fatty liver disease

Veerle Bieghs et al. Hepatobiliary Surg Nutr. 2014 Dec.

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and covers a disease spectrum ranging from steatosis to inflammation, fibrosis, cirrhosis and hepatocellular carcinoma (HCC). The innate immune response in the liver plays an important role during NAFLD progression. In addition, changes in the intestinal microbial balance and bacterial translocation can further affect disease progression. Immune cells in the liver recognize cell damage or pathogen invasion with intracellular or surface-expressed pattern recognition receptors (PRRs), subsequently initiating signaling cascades that trigger the release of factors promoting the inflammatory response during NAFLD progression. Therefore, mechanisms by which cells of the immune system are activated and recruited into the liver and how these cells cause injury and stress are important for understanding the inflammatory response during NAFLD.

Keywords: Liver inflammation; gut-liver axis; inflammasome; innate immunity; toll-like receptors (TLRs).

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Figures

Figure 1
Figure 1
Gut-liver interactions during NAFLD progression. Obesity is associated with intestinal dysbiosis and increased gut permeability. Therefore, microbial products can translocate via the portal circulation to the liver and activate pattern recognition receptors (PRRs). Activated PRRs can trigger the production of pro-inflammatory cytokines, thereby promoting the recruitment of immune cells and stimulating the inflammatory response, fibrogenesis and metabolic stress during NAFLD progression. NAFLD, non-alcoholic fatty liver disease.
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