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Alcohol-associated hepatitis (AH) remains one of the most severe and life-threatening manifestations of alcohol-related liver disease (ALD). It is characterised by rapid onset, limited treatment options and high short-term mortality.1 One of the pathological hallmarks of AH is excessive activation of hepatic inflammatory signalling, notably accompanied by massive neutrophil infiltration in the liver. It has been well documented that under the conditions of alcohol-induced hepatic stress, the liver microenvironment becomes increasingly pro-inflammatory. Hepatocytes, in response to cytokine stimulation, particularly tumour necrosis factor-α and interleukin-1 β, are induced to secrete chemokines, such as C-X-C motif chemokine ligand 1 (CXCL1) and CXCL8 (also known as interleukin-8).2 3 These chemokines are potent chemoattractants that recruit neutrophils from the circulation to the liver. In addition, alcohol-induced hepatocyte injury promotes the activation of liver sinusoidal endothelial cells, leading to the upregulation of the expression of adhesion molecules, including intercellular adhesion molecule 1 and vascular cell adhesion molecule-1, which enhance neutrophil adhesion and transmigration into the inflamed liver tissue.4 This step is crucial for the accumulation of neutrophils in the liver and the progression of inflammatory injury. Moreover, sterile inflammation, initiated by cellular damage and necrotic death of hepatocytes without pathogens, results in the release of damage-associated molecular patterns, including mitochondrial DNA and high mobility group protein-1 (HMGB1). These endogenous danger signals further amplify the inflammatory cascade by activating pattern recognition receptors on immune cells and enhance neutrophil infiltration.5 6 Together, these mechanisms create a self-sustaining loop of hepatocellular injury and immune activation, underscoring the central role of neutrophils in AH pathogenesis (figure 1).