Abstract
BACKGROUND: Although liver is the organ most often associated with the damaging effects of chronic alcohol abuse, other organs may also be affected. In the past decade, data emerged linking chronic alcohol intake to lung dysfunction. However, the mechanisms by which alcohol affects the lung remain incompletely elucidated. METHODS: In this issue, Sueblinvong and colleagues explore the effect of chronic alcohol intake in the well-known rodent model of bleomycin-induced lung injury. This represents a review of their article and a commentary on its findings in relation to current knowledge in the field. RESULTS: The investigators found that chronic alcohol intake increased lung fibrosis in the bleomycin-model of lung injury. This effect was related to increased production of transforming growth factor β (TGFβ) and expression of α-smooth muscle actin. Diet supplementation with S-adenosylmethionine greatly reduced the effect. These data strengthen published reports linking chronic alcohol intake with TGFβ overproduction and lung disrepair after injury, while implicating oxidant stress as a critical mediator of these effects. CONCLUSIONS: A review of Sueblinvong and colleagues' article and the literature strongly suggests that the lung is a target for alcohol, and that chronic alcohol intake may predispose the lung to disrepair after injury. The overexpression of pro-fibrotic growth factors and pro-inflammatory cytokines, and the generation of oxidant stress may lead to lung cellular dysfunction, aberrant tissue remodeling, and loss of lung function. These events may represent targets for intervention, but translational studies evaluating their role in humans are desperately needed.