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目的探讨LIGHT分子在鹦鹉热衣原体(Chlamydia psittaci,Cps)呼吸道感染过程中的作用。方法 C57BL/6J野生型(Wild type,WT)和LIGHT基因敲除(Knock out,KO)小鼠经鼻内接种4.5×10~5 IFU Cps,每天观察记录小鼠的进食、活动、体重变化及生存情况。感染后第4、9、14 d分批处死小鼠,分离肺组织,检测肺组织中Cps载量、病理损伤程度。结果与WT小鼠相比,LIGHT KO小鼠出现更严重的呼吸道感染症状,死亡率更高,肺组织匀浆中Cps载量更高且带菌时间延长,肺部病理损伤程度也显著高于WT小鼠。结论 LIGHT基因缺失可促进Cps呼吸道感染。
Objective To investigate the role of LIGHT in the respiratory tract infection of Chlamydia psittaci (Cps). Methods C57BL / 6J wild type (WT) and LIGHT knockout (KO) mice were inoculated intranasally with 4.5 × 10 ~ 5 IFU Cps. The changes of food intake, activity and body weight were observed daily. Survival. Mice were sacrificed on the 4th, 9th and 14th day after infection, and the lung tissues were separated and the Cps load and the pathological damage degree were detected. Results Compared with WT mice, LIGHT KO mice developed more severe symptoms of respiratory tract infection with higher mortality, higher Cps loading and longer carriage time in lung homogenates, and significantly higher lung pathological damage than WT Mouse. Conclusion LIGHT gene deletion can promote Cps respiratory tract infection.