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

为探讨柴油车尾气颗粒物(DEP)对自身免疫病模型--胶原性关节炎(CIA)的影响。将经完全弗氏佐剂乳化的II型胶原(CII)皮下注射至TALL基底部(第0天)，然后于第21天注射佐剂，诱导出CIA。从第0天到第20天，每隔2天鼻内注射不同剂量的DEP。结果表明，DEP的应用既增加了CIA的发生率，也增加了CIA的严重程度，疾病的加强与抗CIIIg G和Ig G2a抗体的产生有关。DEP还能增强脾细胞对CII的增殖反应。在DEP处理的小鼠中，淋巴细胞显著分泌干扰素-γ、IL-2和IL-4。在CIA发病后给予DEP也有效地提高了疾病的严重程度，以及抗CIIIg G和Ig G2a抗体的产生以及干扰素-γ、IL-2和IL-4的分泌。这些结果表明，接触DEP可能会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.