Health risks have been closely related to increased exposure of fine particulate matter (PM2.5) in general population. Immune system is considered to be a most vulnerable target for airborne pollutants. PM2.5 could make some serious damages to the body organs by inducing immunotoxicity. However, the underlying molecular mechanisms are still unclear. The purpose of this study is aimed to elucidate the possible mechanisms of PM2.5-mediated immunotoxicity on spleen organ by using SD rat models. This research demonstrated that the spleen structure damage induced by PM2.5 treatment was more pronounced in winter than in summer. Mechanistically, TUNEL staining show a considerable increase in spleen apoptosis by summer and winter PM2.5 exposures compared with control. However, winter PM2.5 exposure caused more toxicity in the spleen than summer PM2.5 exposure. Furthermore, our results illustrated that PM2.5 triggered oxidative stress and ERS in spleen tissues of SD rats, and lead to apoptosis via upregulation of CHOP and caspase-12. Likewise, the protein levels of LC3 were significantly increased and p62 was decreased by PM2.5 exposure, thereby activated the autophagy of spleen in SD rats in a concentration-dependent manner. In conclusion, this study supported that PM2.5 mediated the immunotoxicity by the occurrence of stimulation of ERS and autophagy in SD rats. Taken together, these findings suggest PM2.5 as potential agent of immunotoxicity that needs an urgent attention. Graphical abstract Graphical abstract contains poor quality of text inside the artwork. Please do not re-use the file that we have rejected or attempt to increase its resolution and re-save. It is originally poor, therefore, increasing the resolution will not solve the quality problem. We suggest that you provide us the original format. We prefer replacement figures containing vector/editable objects rather than embedded images. Preferred file formats are eps, ai, tiff and pdf.Thanks you attention. We will provide tiff format image.
Keywords: Apoptosis; Autophagy; ERS; Oxidative stress; PM2.5; Spleen.