Mechanisms of zidovudine-induced mitochondrial toxicity and myopathy
Guevara IL, Pandya AG
In ALD, multiple liver cells including HSCs, KCs, Th17 cells, LSECs and hepatocytes, along with DAMPs and PAMPs, collaborate to prime, activate and recruit neutrophils to the liver.47 48 Alcohol-induced liver damage triggers the release of these molecular signals, which initiate an inflammatory cascade, leading to neutrophil infiltration.47 48 This process is particularly pronounced in patients with AH, where large numbers of neutrophils accumulate in the liver and contribute to liver injury, largely through excessive ROS production.48 ROS, while essential for pathogen elimination, can also cause significant oxidative stress, damaging hepatocytes and contributing to the progression of liver inflammation and injury in ALD.48 However, recent research has highlighted the dual role of neutrophils in ALD, showing that while they contribute to liver injury, they are also involved in resolving inflammation and promoting tissue repair.4951 Neutrophils destroy pathogens and clear cellular debris through phagocytosis48 and play a critical role in shaping the immune environment by influencing macrophage polarisation.50 Specifically, neutrophils can promote the transition of macrophages from a pro-inflammatory M1 phenotype to an anti-inflammatory M2 phenotype, thereby aiding in the resolution of liver inflammation.50 This functional plasticity suggests that neutrophils may help to fine-tune the immune response in ALD, balancing pro-inflammatory and tissue-repairing activities
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