Histone modification in the lung injury and recovery of mice in response to PM2.5 exposure

Epidemiological and experimental studies have progressively provided a better knowledge of the underlying mechanisms by which fine particulate matter (PM2.5) exerts its harmful health effects. However, limited studies focused on the effect and following recovery after the particulate exposure ended. In this study, we determined PM2.5 exposure-caused effects on the lung and their recovery in mice after terminating aspiration, and clarified the possible molecular modification. The results revealed that PM2.5 exposure for 4 weeks significantly decreased the lung function, and the changes returned to normal levels after 1-week recovery. However, we observed persistent particle alveolar load following 2-week recovery. Interestingly, the alterations of H3K27ac expression and related enzyme activities mimicked the changes of respiratory function during the process, and chromatin immunoprecipitation-seqences (ChIP-seq) suggested that these PM2.5-associated differential H3K27ac markers participated in immune responses and chemokine signaling pathway with stat2 and bcar1 being two important genes. Consistently, the expression of pro-inflammatory cytokines and chemokines elevated after PM2.5 exposure for 4-week, and reversed to normal levels following 2-week recovery. The study highlighted that PM2.5 aspiration caused histone modification associated lung dysfunction and inflammation, and the action restored after exposure ending and 2-week recovery. Also, persistent particle alveolar load might be a long-term potential risk for lung diseases.