In Vitro Exposure To Cigarette Smoke Activates Eosinophils: Implications For Lung Inflammation

Abstract

Effects of cigarette smoke (CS) on eosinophils (EOS), important cells involved in the pathogenesis of chronic lung diseases such as asthma, were studied in vitro. EOS were isolated from healthy and mildly atopic donors and exposed to soluble components of cigarette smoke (CSE). Viability and apoptosis were assessed by flow cytometry after staining with propidium iodide and Annexin-V. Activation was determined by release of newly-synthesized (IL-8, IL-6) mediators and by phosphorylation of MAPKs. CSE effects on ultrastructural morphology and production of neutrophil chemotactic factors in CSE-activated EOS were also evaluated. CSE concentrations from 0-2.5% were non-toxic for up to 18-24 hours of exposure. However, CSE at 2.5% activated EOS as evidenced by ultrastructural degranulation: release of IL-8 and IL-6, and increased expression of the MAPK, c-Jun. Supernatants from CSE-activated EOS were found to be significantly chemotactic for neutrophils. These results suggest that CS may aggravate lung inflammation by activating EOS which, in turn, release inflammatory mediators promoting inflammatory cell recruitment and lung remodeling.