Ethanol (EtOH)-induced TGF-β1 and reactive oxygen species production are necessary for EtOH-induced alveolar macrophage dysfunction and induction of alternative activation.

ABSTRACT:

Background

Previous studies have shown that chronic ethanol (EtOH) ingestion results in impaired alveolar macrophage function, increased TGF-β(1) production, and decreased antioxidant availability. Similarly, alternative activation (M2 activation) of alveolar macrophages also induces TGF-β(1) production and impairs macrophage function. However, the potential links between EtOH-induced alveolar macrophage derangements, M2 activation, TGF-β(1) production signaling, and oxidant stress have yet to be examined. We hypothesized that EtOH-induced oxidant stress and induction of TGF-β(1) signaling result in alternative activation which subsequently impairs the phagocytic capacity of alveolar macrophages.

Methods

Primary rat alveolar macrophages and the alveolar macrophages cell

SUBMITTER: Brown SD 

PROVIDER: S-EPMC3414680 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature