Imbalance of Th1 and Th2 cells in cardiac injury induced by ambient fine particles

The study was to explore the potential immunoregulatory mechanisms linking fine particles and cardiac injury. Wistar kyoto (WKY) rats were exposed by intratracheal instillation to fine particles with the doses of 0.0, 1.6, 8.0 and 40.0 mg/kg b.w., respectively. The exposure was conducted once a day, for three consecutive days. Twenty-four hours after the last exposure, the rats were sacrificed. Th1- and Th2-related transcription factors and cytokines were assessed in left ventricle of rats. The mRNA expressions of Th1- and Th2-related transcription factors signal transducer and activator of transcriptionl 1 (STAT1), signal transducer and activator of transcriptional 6 (STAT6), GATA-3 and T-bet were assessed in left ventricle of rats using real-time PCR. Meanwhile, the levels of Th1- and Th2-related cytokines IL-4, IL-13 and interferon gamma (IFN-γ) were determined by ELISA kits in cardiac homogenate supernatant of rats. Furthermore, the protein expression of IL-4 and IFN-γ were detected in myocardium by Western blot. The results of cardiac histology demonstrated exacerbated cardiac lesions and histological characterization of inflammation and degeneration in rats after exposure to fine particles. Moreover, fine particles induced significant increase of IL-4 and IL-13 and decrease of IFN-γ in myocardium of rats. The mRNA expression of STAT1, STAT6 and GATA-3 were up-regulated in left ventricle of rats in a dose-dependent manner, whereas T-bet was significantly down-regulated. The variations of these cytokines demonstrated the imbalance of Th1 and Th2 cytokines existed in cardiac injuries induced by fine particle. The imbalance of Th1/Th2 cytokines might be one of the mechanisms of immunotoxicity of cardiovascular system induced by ambient fine particles.

► Fine particles caused imbalance of Th1 and Th2.
► Fine particles may skew cytokine production toward a Th2 pattern.
► Rats exhibited marked increase in IL-4 and IL-13 and decrease in IFN-γ.
► The imbalance of Th1/Th2 might be one of the mechanisms of toxicity of PM2.5.