Alcoholic liver disease: Current insights into cellular mechanisms

Figure 2 The inflammatory response during alcoholic liver disease. Excessive consumption of alcohol causes lipopolysaccharide release from the gut activating toll-like receptor 4 on Kupffer cells (KCs). Pattern recognition receptors become activated by pathogen-associated molecular patterns/damage-associated molecular patterns which induces inflammation via release of proinflammatory cytokines and inflammasome activation. Interleukin (IL)-18 production from KCs causes activation of natural killer cells. Toll-like receptor stimulation in hepatic stellate cells results in the expression of IL-6, transforming growth factor-β1 and tumor necrosis factor-α. (Figure created with BioRender.com). DAMPs: Damage-associated molecular patterns; FFA: Free fatty acids; PAMPs: Pathogen-associated molecular patterns; IL: Interleukin; LPS: Lipopolysaccharide; NF-κB: Nuclear factor-κB; NK: Natural killer; NLRP3: NOD-, LRR- and pyrin domain-containing protein 3; PRR: Pattern recognition receptor; ROS: Reactive oxygen species; TGF-β: Transforming growth factor β; TLR4: Toll-like receptor 4; TNF-α: Tumor necrosis factor-α.