Abstract 595: Gender Difference Was Present in the Production of Cytokines in Mice With PM Exposure

Abstract

Gender difference is present in a variety of diseases especially cardiovascular diseases like coronary artery diseases ( CAD ). It is well known that males tend to suffer from CAD earlier than females for largely unknown reasons. Oxidative stress and inflammation are considered an important mechanism for the development of cardiovascular diseases. Cytokines including interleukin (IL)-6 and tumor necrosis factor-α (TNF-α) play an important role in oxidative stress and inflammation. Ambient fine particulate matter ( PM ) exposure is closely associated with cardiovascular diseases and oxidative stress. The present study was designed to determine if there was a gender difference in the production of cytokines in the mice with PM exposure. Both male and female wild-type C57BL/6 mice (8-10 weeks) were exposed to PM2.5 for 6 weeks via intranasal approach with PBS as the control. Serum concentrations of the cytokines including IL-6, IL-1β, and TNF-α were measured with ELISA in the mice before and after PM exposure. There was no difference between male and female mice in the serum levels of IL-6, IL-1β, or TNF-α at the baseline. As expected, PM exposure substantially increased the serum levels of IL-6, IL-1β, and TNF-α both in male and female mice (by up to 6 times). However, their serum concentrations were significantly higher in male mice than in the females by 64.2%, 26.5%, and 30.7% for IL-6, IL-1β, and TNF-α, respectively (p < 0.05, n = 10). Similar changes in the inflammatory infiltrations in the lungs were observed in the male and female mice with PM exposure. The data from the present study demonstrated that more cytokines were produced in male mice than in the females with PM exposure. The clear gender difference in the serum levels of cytokines in response to PM exposure may partially contribute to the gender difference in the development of cardiovascular diseases. Further studies are needed to investigate the mechanisms related to the gender difference in the response to PM exposure.