| 肿瘤坏死因子α在抗鼠衣原体生殖道感染过程中的作用 |
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| 引用本文： | 陈 曦,刘璐瑶,张 旭,陆春雪,陈 利,全淑芬,陈丽丽.肿瘤坏死因子α在抗鼠衣原体生殖道感染过程中的作用[J].南方医科大学学报,2020,40(3):388-393. |
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| 作者姓名： | 陈 曦 刘璐瑶 张 旭 陆春雪 陈 利 全淑芬 陈丽丽 |
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| 摘 要： | 目的 探讨肿瘤坏死因子α（TNF-α）在抗衣原体感染免疫以及介导衣原体生殖道病理损伤过程中的作用。方法 以5~6周龄雌性C57BL/6J野生型小鼠及TNF-αR基因敲除小鼠为研究对象，野生型和TNF-αR基因敲除两组各15只小鼠，经生殖道感染1×104包涵体形成单位的鼠衣原体，初次感染后第56天，每组8只小鼠再次感染同等剂量的鼠衣原体。每隔3~4 d 取小鼠生殖道分泌物用于衣原体包涵体数目的检测。于初次感染后第80天处死小鼠，收集小鼠腹腔巨噬细胞，并分离生殖道和脾脏。观察输卵管和子宫角病理损伤程度，并采用盲法对管腔扩张以及炎性细胞浸润程度进行半定量分析；测定小鼠巨噬细胞培养上清中的IL-6、IL-8、IL-1α、IL-1β和TNF-α等前炎症因子水平；制备脾细胞悬液，体外经衣原体EB刺激后检测其产生的IL-4、IL-5、IL-17和 IFN-γ 等细胞因子水平。结果 TNF-αR 基因敲除组生殖道衣原体清除速度与野生型组基本一致，与初次感染或再次感染无
关；两组小鼠子宫角和输卵管的炎症程度差异没有统计学意义（P>0.05），但TNF-αR基因敲除组输卵管水肿程度明显低于野生型组（P<0.05）。腹腔巨噬细胞细胞因子检测结果显示，TNF-αR基因敲除小鼠的TNF-α水平高于野生型小鼠（P<0.05）；脾细胞细胞因子水平显示，两组小鼠脾细胞均产生较高水平的IFN-γ，TNF-αR基因敲除小鼠产生的IL-17细胞因子水平低于野生型小鼠（P<0.05）。结论 TNF-α对小鼠生殖道清除鼠衣原体感染无影响，但可促进鼠衣原体引起的生殖道炎症病理损伤。
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Role of tumor necrosis factor-α in Chlamydia Muridarum infection in the urogenital tract
of mice |
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| Abstract: | Objective To explore the role of tumor necrosis factor-α (TNF-α) in immune response to urogenital chlamydial
infection and urogenital pathology in mice. Methods Fifteen female wild-type (WT) C57BL/6J mice and 15 TNF-α receptor
knockout (TNF-αR KO) mice were inoculated intravaginally with 1×104 inclusion forming units (IFUs) of live C. muridarum. At
56 days after the first inoculation, 8 mice from each group were subjected to a second inoculation at the same dose. Vaginal
swabs were taken every 3 or 4 days to detect the number of inclusion bodies of chlamydia. On day 80 after the first inoculation,
the mice were euthanized and peritoneal macrophages were collected and the vaginal tract and spleen were dissected. The
pathologies in the fallopian tube and the uterine horn were observed and the severity of inflammatory cell infiltration and
lumen dilatation were semi-quantitatively scored. The levels of interleukin-6 (IL-6), IL-8, IL-1α, IL-1β and TNF-α in the
supernatant of the peritoneal macrophage were detected. Spleen cell suspension was prepared, and after stimulation with
chlamydia EB in vitro, the levels of the cytokines including IL-4, IL-5, IL-17 and interferon-γ (IFN-γ) were determined in the
cells. Results The clearance rate of Chlamydia from the urogenital tract was similar between TNF-αR KO mice and WT mice
regardless of the primary or second infection. The severity of inflammation in the fallopian tube and the uterine horn did not
differ significantly between the two groups, but TNF-αR KO mice had significantly milder dilation of the fallopian tubes (P< 0.05). The peritoneal macrophages from TNF-αR KO mice produced a significantly higher level of TNF-α than those from WT
mice (P<0.05); the spleen cells from the two groups both produced high levels of IFN-γ, but IL-17 production by the spleen
cells was significantly lower in TNF-αR KO mice than in WT mice (P<0.05). Conclusion TNF-α is not associated with
protective immune response against C. muridarum infection, and can worsen the inflammatory damages of the urogenital tract
caused by C. muridarum in mice. |
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