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The production of reactive oxygen species (ROS) by activated macrophages and neutrophil granulocytes represents an important cause of alcohol-induced oxidative stress and significantly contributes to the pathogenesis of alcoholic liver disease (ALD).1 Furthermore, diffuse neutrophil infiltration of the liver is a key feature of acute alcoholic hepatitis actively participating to parenchymal injury.2 However, during ALD progression to cirrhosis, neutrophil functions such as ROS production, bacterial phagocytosis and granule exocytosis are impaired leading to an increased susceptibility to bacterial infections of cirrhotic patients.3 Indeed, the development of bacterial peritonitis is a common complication of cirrhosis, while sepsis is a major cause of mortality in patients with decompensated alcoholic cirrhosis being also associated with multiorgan failure and immune deficiencies.4
The key role of neutrophils in antibacterial defences mainly relies on the capacity of the enzyme NADPH oxidase 2 (NOX2) to generate superoxide anion (O2 −) during a process known as oxidative burst. Superoxide anion, in fact, by conversion to hydrogen peroxide, fuels myeloperoxidase-mediated production of the powerful bactericidal agents, hypochlorite and chloramine.5 NOX2 is a multiprotein enzymatic system consisting of the transmembrane proteins gp91 phox and p22 phox forming the …
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
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