Yoshino S, Sagai M
Department of Microbiology, Saga Medical School, Saga 849-8501, Japan.
J Pharmacol Exp Ther. 1999 Aug;290(2):524-9.
The present study was undertaken to investigate the effect of diesel exhaust particles (DEP) on collagen-induced arthritis (CIA), which is an experimental model of autoimmune disease, in mice. CIA was induced by s.c. injection of type II collagen (CII) emulsified with complete Freund's adjuvant into the base of the tail (day 0) followed by a booster injection on day 21. Varying doses of DEP were intranasally administered every 2 days from days 0 to 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 interferon-gamma, interleukin (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 interferon-gamma, IL-2, and IL-4. These results suggest that exposure to DEP may influence autoimmune disease.
本研究旨在探讨柴油废气颗粒（DEP）对小鼠胶原诱导性关节炎（CIA）的影响，CIA是一种自身免疫性疾病的实验模型。通过在小鼠尾部基部皮下注射用完全弗氏佐剂乳化的II型胶原（CII）（第0天）诱导CIA，随后在第21天进行加强注射。从第0天到第20天，每2天经鼻给予不同剂量的DEP。结果表明，给予DEP增加了CIA的发病率和严重程度。疾病的加重与抗CII IgG和IgG2a抗体的显著产生有关。DEP处理还增强了脾细胞对CII的增殖反应。DEP处理的小鼠的淋巴细胞显著分泌γ干扰素、白细胞介素（IL）-2和IL-4。在CIA发病后给予DEP也有效地加重了疾病的严重程度，以及抗CII IgG和IgG2a抗体的产生和γ干扰素、IL-2和IL-4的分泌。这些结果表明，接触DEP可能影响自身免疫性疾病。
