摘要目的：探讨IL-12和IL-23在抗衣原体泌尿生殖道感染免疫及病理损伤中的作用。方法用1×104 IFU的鼠肺炎型沙眼衣原体（ MoPn）经生殖道感染野生型（ wt）、IL-12p35 KO和IL-12p40 KO小鼠，每组一半小鼠于感染后114 d，再次感染相同剂量的MoPn。每隔3～4 d取生殖道分泌物，测定其中衣原体包涵体的数量。原发感染后114 d或143 d，处死小鼠，分离泌尿生殖道，肉眼观察其肾脏、输卵管、子宫角水肿程度，并切片， HE染色后，显微镜下观察各组织炎性浸润程度和管腔水肿程度，并计数肾组织中衣原体和细菌数量。结果在MoPn原发感染后，IL-12p35 KO和IL-12p40 KO小鼠清除衣原体的速度相当，带菌时间均较wt小鼠明显延长。所有小鼠均出现严重的上生殖道组织病变，但KO小鼠和wt小鼠病变程度没有明显差异。几乎所有IL-12p40 KO和部分IL-12p35 KO小鼠均发生严重的肾脏病变，而wt小鼠肾脏未见明显异常。在KO小鼠病变的肾组织匀浆及切片中均能检测到衣原体抗原，且包涵体数量均显著高于wt小鼠。结论 IL-12和IL-23可限制经生殖道感染的MoPn扩散到肾脏，IL-12或IL-23基因缺失后生殖道衣原体感染易并发肾脏病变。

abstractsAbstract] Objective To study the roles of IL-12 and IL-23 in the development of protective im-munity and pathological changes during chlamydial urogenital infection.Methods C57BL/6J wild type (wt) mice and mice deficient in IL-12p35 (IL-12p35 KO) or IL-12p40 (IL-12p40 KO)were inoculated in-travaginally with 1×104 IFU of live Chlamydia muridarum ( C.muridarum) organisms.Half mice of each group were reinfected on day 114 after primary infection.Vaginal swabs were taken every 3 or 4 days to mo-nitor live organism shedding.The mice were sacrificed after 114 or 143 days of primary infection and the va-ginal tract and kidney samples were collected for pathological analysis.The numbers of chlamydial inclusion bodies and bacteria in kidney homogenates were titrated after 100 days of primary infection.Results The infection time courses of mice deficient in either IL-12p35 or IL-12p40 were similar after primary infection, but were prolonged as compared with the wild type mice.All mice regardless of genotypes developed severe pathological damages in upper genital tracts with no significant difference among different groups.Almost all IL-12p40 KO mice and some IL-12p35 KO mice showed pathological changes in kidney samples.No obvious abnormality was observed in any of the kidneys from wild type mice.Neither the age-matched IL-12p35 KO nor IL-12p40 KO mice developed any gross pathological changes in kidney in the absence of chlamydial in-fection.C.muridarum inclusions were detected in kidney samples with gross pathological damages from IL-12p35 KO mice and IL-12p40 KO mice.No inclusions were ever detected in kidneys from the wild type mice.The numbers of chlamydial inclusions in the IL-12p40 KO mice were much higher than those of the IL-12p35 KO mice.Live bacteria were detected in mice deficient in either IL-12p35 or IL-12p40, but not in the wild type mice.No significant difference with the number of live bacteria was found between IL-12p35 KO mice and IL-12p40 KO mice.Conclusion IL-12 and IL-23 could inhibit the spread of C.muridarum in-fection from genital tract to kidney.The deficiency of IL-12 or IL-23 might relate to the renal lesions induced by Chlamydia infection.