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pneumoniae protein, alveolar macrophages and peripheral blood mononuclear cells obtained both from people with AUD and people without AUD exhibited a dose- and time-dependent increase in proinflammatory cytokine production, with no differences between the two groups.60 Treatment with the potent antioxidant N-acetylcysteine reduced cytokine production from both cell types, except for IL-1beta, which remained elevated in cells obtained from people with AUD.60 These data suggest that alcohol misuse alters the basal inflammatory profile of macrophages and that mitigation of oxidative stress with N-acetylcysteine partially reverses proinflammatory cytokine secretion in macrophages obtained from individuals with AUD

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