Crotonaldehyde induces apoptosis and immunosuppression in alveolar macrophages

Crotonaldehyde, a highly toxic α, β-unsaturated aldehyde, is a major component of cigarette smoke (CS) and a ubiquitous environmental pollutant. Exposure to crotonaldehyde-rich pollutants such as CS is associated with suppression of respiratory host defense against infections. The aim of this study was to evaluate the apoptotic and immunological effects of crotonaldehyde exposure in a rat alveolar macrophage (AM) cell line, NR8383. Our studies showed that crotonaldehyde induced AM cell death mainly via the apoptotic process. Crotonaldehyde also decreased the phagocytic activity of AMs. Crotonaldehyde caused inhibition of NO, TNF-α, IL-1β and IL-12 production in AMs treated with lipopolysaccharide (LPS), which is probably related to inhibition of NF-κB activation. These results indicate that crotonaldehyde can cause adverse effects in AMs via multiple mechanisms, and may contribute to compromised lung immunological response in smokers.

► Crotonaldehyde induced AM cell death mainly via the apoptotic process. ► Crotonaldehyde decreased the phagocytic activity of AMs. ► Crotonaldehyde caused inhibition of NO, TNF-α, IL-1β and IL-12 production in AMs treated with LPS. ► Crotonaldehyde-induced inhibition of inflammatory mediators release is probably related to inhibition of NF-κB activation.