树突状细胞在沙眼衣原体小鼠肺炎株呼吸道感染中免疫保护作用的研究  

Immunoprotective role of dendritic cells in Chlamydia muridarum respiratory infection

作　　者：孙若元 檀露 查晓宇 脱雨晴 杨帅妮 曾佳佳 许悦悦 张虹 曲同兴 张学军 白虹 Sun Ruoyuan;Tan Lu;Zha Xiaoyu;Tuo Yuqing;Yang Shuaini;Zeng Jiajia;Xu Yueyue;Zhang Hong;Qu Tongxing;Zhang Xuejun;Bai Hong(Tianjin Key Laboratory of Cellular and Molecular Immunology,Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China,Department of Immunology,School of Basic Medical Sciences,Tianjin Medical University,Tianjin 300070,China)

机构地区：[1]天津医科大学基础医学院免疫学系,国家教育部免疫微环境与疾病重点实验室,天津市细胞和分子免疫学重点实验室,天津300070

出　　处：《中华微生物学和免疫学杂志》2023年第2期123-129,共7页Chinese Journal of Microbiology and Immunology

基　　金：国家自然科学基金(31870889);天津市自然科学基金(19JCZDJC35800,18JCZDJC98300)。

摘　　要：目的探讨树突状细胞(dendritic cells,DC)在沙眼衣原体小鼠肺炎株(Chlamydia muridarum,Cm)呼吸道感染中的作用以及对适应性免疫应答的影响。方法C57BL/6小鼠经鼻腔吸入1×10^(3)包涵体形成单位(inclusion-forming units,IFU)Cm建立小鼠呼吸道感染模型。流式细胞术检测感染后0、3、7 d脾组织中总CD11c^(+)MHCⅡ^(+)DC比例和共刺激分子(CD40、CD80和CD86)表达情况;qPCR检测小鼠脾组织中DC细胞因子IL-12p40、IL-10和IL-6 mRNA的表达;磁珠分选出Cm感染后7 d的小鼠脾组织DC并过继转移给受体小鼠,于感染后14 d利用细胞内细胞因子染色检测受体小鼠Th1应答水平。结果Cm感染诱导小鼠脾组织DC大量浸润并且共刺激分子表达增加;脾组织DC细胞因子IL-12和IL-10 mRNA的表达在感染后3 d达到高峰;将Cm感染小鼠脾组织DC过继转移给受体小鼠,受体小鼠感染Cm后疾病减轻,肺组织衣原体繁殖降低,且肺和脾组织中的Th1细胞比例显著升高。结论DC在Cm感染后成熟、活化并促进Th1细胞免疫应答,在衣原体呼吸道感染中发挥免疫保护作用。Objective To investigate the role of dendritic cells(DC)in Chlamydia muridarum(Cm)respiratory infection and their effect on adaptive immune response.Methods C57BL/6 mice were exposed to 1×10^(3)inclusion-forming units(IFU)of Cm through inhalation to establish the mouse model of Cm respiratory infection.The proportion of CD11c^(+)MHCⅡ^(+)DC and the expression of costimulatory molecules(CD40,CD80 and CD86)in spleen tissues were detected by flow cytometry on 0,3 and 7 d after infection.The expression of IL-12p40,IL-10 and IL-6 at mRNA level in spleen tissues was detected by qPCR.Mouse splenic DC isolated on 7 d after Cm infection were sorted by magnetic beads and then transferred to recipient mice.Th1 response in the recipient mice was measured using intracellular cytokine staining 14 d after infection.Results Cm respiratory infection induced massive infiltration of DC and promoted the expression of costimulatory molecules on splenic DC.The expression of IL-12 and IL-10 at mRNA level in splenic DC reached the peak on 3 d after infection.Transferring the splenic DC of Cm-infected mice into the recipient mice could alleviate the disease condition in the recipient mice after Cm infection with reduced Cm inclusion-forming units in lung tissues and significantly increased proportion of Th1 cells in lung and spleen tissues.Conclusions Cm respiratory infection could induce the maturation and activation of DC,which promoted Th1 immune response.DC played an important role in Cm infection.

关 键 词：免疫 沙眼衣原体小鼠肺炎株 树突状细胞 TH1免疫应答 

分 类 号：R563.1[医药卫生—呼吸系统]