Fig. 1
From: Immunological mechanisms and emerging therapeutic targets in alcohol-associated liver disease
Triggers of Immune Response in ALD. Acetaldehyde and reactive oxygen species (ROS) generated during alcohol metabolism activate inflammatory signaling pathways, leading to hepatocyte injury, apoptosis, and necrosis. These events trigger the release of inflammatory mediators and damage-associated molecular patterns (DAMPs). Chronic alcohol consumption disrupts the intestinal barrier, increasing permeability and facilitating gut-derived microbial products’ translocation to the liver via the portal vein, thereby initiating an immune response. The nervous system modulates hepatic immune cell phenotypes through sympathetic signaling and neurotransmitters. Additionally, adipose-liver crosstalk, mediated by cytokines, adipokines, and metabolic signals, further amplifies immune activation and promotes the release of pro-inflammatory cytokines and chemokines. Collectively, these inter-organ interactions drive liver inflammation, exacerbate hepatocellular damage, and contribute to the progression of ALD
