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... by phagocytosing the apoptotic cells and their inflammatory cytokine production is increased [9]. Alcohol consumption promotes liver inflammation by increasing the translocation of gut-derived endotoxins to the portal circulation and activating Kupffer cells through the LPS/Tolllike receptor (TLR) 4 pathways. ALD is associated with imbalanced immune responses and increased production of proinflammatory cytokines and chemokines [10, 11]. Various cytokines are associated with ALD, including hepatoprotective cytokines, such as lnterleukin-6 (IL-6), and anti-inflammatory cytokines, such as IL-10 [12]. These two cytokines are produced by ethanol-induced LPS-stimulated Kupffer cells and can attenuate alcohol-induced liver injury. Inflammasome and several chemokines also contribute to ALD. 2 Mediators of Inflammation Ethanol consumption Fatty liver Abstinence Abstinence Cure Alcoholic hepatitis Severity Death HCC Liver fibrosis cirrhosis Liver Liver failure 90–100% 30–40% 10–20% 10–30% 3–10% Figure 1: The natural history of alcoholic liver disease. Chronic ethanol consumption leads to fatty liver for more than 90%. But only up to 40% of this population develops more severe forms of alcoholic...

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...shipsbetween oxidative stress, cytokines and hepatic fatty acid metabolism in alcoholic liversdisease.sThe role of STAT3, another transcription factor in alcoholic liver injury has beensinvestigated (=-=Gao, 2005-=-). Compared with wild-type mice, Kupffer cells from alcohol-fedshepatocyte-specific STAT3KO mice produced similar amounts of ROS and hepaticsproinflammatory cytokines compared to control mice. On the ...

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...of the liver is to detoxify the organism. Consequently, hepatocytes are constantly subjected to diverse infectious or toxic agents that can generate liver damage and initiate an inflammatory response =-=[15]-=-. The purpose of local inflammation is to clear the damage by activating apoptosis of affected hepatocytes, and to promote repair of the tissue by activating cell proliferation [12]. Under normal cond...

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...ork D (Additional data file 1, D) with the up-regulation of STAT1, one of the major components of the type I IFN transduction pathway, playing a key role in antiviral defense, inflammation and injury =-=[32]-=- and the up-regulation of complement C3 with a role in innate immunity as well as in acute phase response [33]. This network also included the EGFR-like receptor ERRB3 associated with cell survival an...

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...fection, alcoholic and non-alcoholic steatohepatitis [14,16]. Various factors can active hepatic STAT3 signaling such as inflammatory cytokines, growth factors, hormones, and hepatitis viral proteins =-=[17]-=-. Several cytokines (such as IL-6, IL-6 family cytokines and IL-22) that activate STAT3 in hepatocytes have been shown to promote HCC cell growth in vivo and in vivo [18,19]. Recently, Park et al. rep...

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...uated when a RhoA inhibitor was added, showing that the RhoA pathway was involved in the effects of arecoline on HA22T/VGH cells. In the liver, STAT3 is mainly activated by IL-6 and related cytokines =-=[15,16]-=-. In the IL-6 signaling pathway, the functional IL-6 receptor complex is composed of an IL-6 receptor that binds IL-6 and a signal transducing Figure 5 The RhoA inhibitor, C3 exoenzyme, abolishes arec...

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...ter PH in this group (Figure 7, A and B). IL-6 plays an important role in the induction of the JAK-STAT3 pathway that contributes to hepatoprotective and hepatomitogenic effects in liver regeneration =-=[34,35]-=-. We, therefore, also determined whether macrophage depletion affects STAT3 activation. Western blotting was performed to detect liver expression of STAT3, phosphor-STAT3 and b-actin. We found that at...

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...ity to various autoimmune diseases, suggesting an association between STAT4 gene polymorphism and autoimmune diseases [17]. STAT4 is considered important in a mouse model of Th1dependent liver injury =-=[18]-=-. Therefore, we hypothesized that STAT4 polymorphisms may overlap in genetic susceptibility between AIH and other autoimmune diseases. To test this hypothesis, we investigated the association of STAT4...