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. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: Hepatology. 2015 Jan 30;61(3):883–894. doi: 10.1002/hep.27489

Figure 7. MLCK contributes to alcoholic liver disease.

Figure 7

MLCK+/+ and MLCK−/− mice were orally fed a control (n = 4) and alcohol diet (n = 10–14). (A) Plasma ALT level. (B) Hepatic triglyceride content. (C) Representative liver sections after hematoxylin-eosin staining. (D) Representative liver sections after oil red O staining. (E) Plasma ethanol concentration. *p < 0.05. (F) Schematic representation of the proposed model of microbial translocation during alcoholic liver disease: Following the onset of alcoholic dysbiosis, monocytes and macrophages of the intestinal lamina propria are activated and produce TNFα. TNFα binds to TNFRI on enterocytes and increases intestinal permeability. This is in part mediated by the activation of MLCK resulting in disruption of tight junctions. Microbial products cross the mucosal barrier to reach the liver via the portal circulation. Microbial products cause hepatic inflammation and liver disease. The model has been reproduced from39 with permission from Elsevier and modified with additional permission from Elsevier.