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目的 :探讨趋化性细胞因子巨噬细胞炎症蛋白 1(MIP 1α)和单核细胞趋化蛋白 1(MCP 1)在沙眼衣原体肺感染中的产生及与机体防御的关系。方法 :用沙眼衣原体小鼠肺炎株 (MoPn)通过鼻腔感染小鼠 ,酶消化法制备小鼠肺组织炎症细胞 ,Wright Giemsa染色计数巨噬细胞占肺炎症细胞的百分率 ;用RT PCR检测小鼠肺组织趋化性细胞因子及细胞因子mRNA表达 ;ELISA法检测肺组织匀浆中细胞因子分泌。结果 :MoPn感染后 7及 14天 ,MIP 1α和MCP 1及其相应的受体CCR1、CCR2在小鼠肺组织中的表达明显增高。与之趋化作用有关的单核 巨噬细胞在肺组织中的浸润也随之增高 ;而且MoPn感染上调Th1细胞因子IFN γ及IL 12的表达及分泌 ,未见Th2细胞因子IL 4在肺组织中的基因表达及分泌 ;但具有免疫抑制作用的Th2细胞因子IL 10在感染后 7天明显表达。结论 :衣原体呼吸道感染诱导CC趋化性细胞因子MIP 1α和MCP 1高表达 ,可能与单核细胞免疫防御及Th1/Th2免疫应答调节有关。
Objective: To investigate the relationship between chemotactic cytokines macrophage inflammatory protein 1 (MIP 1α) and monocyte chemoattractant protein 1 (MCP 1) in lung infection of Chlamydia trachomatis and their relationship with body defense. Methods: Mice were infected by intranasal infection with MoPn and inflammatory cells were isolated by enzymatic digestion. The percentages of Wright Giemsa stained macrophages in lung inflammatory cells were detected by RT PCR. Tissue chemotactic cytokines and cytokines mRNA expression; ELISA assay of lung tissue homogenate cytokine secretion. Results: At 7 and 14 days after MoPn infection, the expression of MIP 1α and MCP 1 and their corresponding receptors CCR1 and CCR2 in lung tissues of mice were significantly increased. The infiltration of mononuclear macrophages correlated with chemotaxis also increased in lung tissues. Moreover, MoPn infection up-regulated the expression and secretion of Th1 cytokines IFNγ and IL-12, but no effect of Th2 cytokine IL-4 on lung tissue However, IL-10, an Th2 cytokine with immunosuppressive effect, was expressed 7 days after infection. Conclusion: Chlamydial respiratory tract infection induces the expression of CC chemokines MIP 1α and MCP 1, which may be related to monocyte immune defense and Th1 / Th2 immune response.