Studies on the effect of diesel exhaust particles on autoimmune disease and its mechanisms

本研究旨在探讨柴油机尾气颗粒（DEP）对自身免疫性疾病小鼠胶原性关节炎（CiA）的影响。用完全的弗氏佐剂乳化的II型胶原（CII）皮下注射到高的底部（第0天），然后在第21天加强注射。从第0天到第20天，每2天鼻内给药不同剂量的DEP。结果表明，DEP可提高CIA的发生率和严重程度。疾病的加重与显著的抗cii IgG和IgG2a抗体的产生有关。DEP治疗也增强了脾细胞对CII的增殖反应。dep处理小鼠淋巴样细胞分泌ifn - γ、IL-2和IL-4。CIA发病后给予DEP也能有效提高疾病的严重程度，提高抗cii IgG和IgG2a抗体的产生以及ifn - γ、IL-2和IL-4的分泌。这些结果表明暴露于DEP可能影响自身免疫性疾病。

The present study was undertaken to investigate the effect of diesel exhaust particles (DEP) on collagen-Induced arthritis (CiA) in mice which Is an experimental model of autolmmune disease. CIA was induced by subcutaneous injection of type II collagen (CII) emulsified with complete Freund's adjuvant Into the base of the tall (day 0) followed by a booster injection on day 21. Varying doses of DEP were intranasally administered every 2 days from day 0 to day 20. The results showed that administration of DEP enhanced both the Incidence and the severity of CIA.The enhancement of the disease was associated with pronounced production of anti-CII IgG and IgG2a antibodies. Treatment with DEP also augmented proliferative responses of spleen cells to CII.There was marked secretion of IFN-gamma, IL-2, and IL-4 from the lymphoid cells in DEP-treated mice. Administration of DEP after onset of CIA was also effective in enhancing the severity of the disease as well as production of anti-CII IgG and IgG2a antibodies and secretion of IFN-gamma , IL-2, and IL-4. These results suggest that exposure to DEP may influence autoimmune disease.