Chen Lili, Sun Yuanbin, Xu Sha, Fu Xizong, Zhou Zhou, Lu Chunxue, Yang Fei, Xu Guilian, Wu Yimou
Wei Sheng Wu Xue Bao. 2015 Apr 4;55(4):492-500.
To study the role of lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells (LIGHT) in the development of protective immunity and pathology during Chlamydia Muridarum urogenital infection in mice.
C57BL/6J wild type (wt) and mice deficient in LIGHT (LIGHT KO) were inoculated intravaginally with 1 x 10(4) IFUs of live C. muridarum organisms. Half mice of each group were reinfected on day 49 after primary infection. We took mice vaginal swabs every 3 or 4 days to monitor live organism shedding. On day 80 after the primary infection, mice were sacrificed, the vaginal tract was isolated for pathology analysis. The spleen cells were collected and IL-4, IL-5, IL-17 and IFN-y were detected by ELISA in the spleen cells culture supernatant after restimulated by UV-MoPn EB. The titers of different Ab isotypes were measured in mice serum by Indirect Immunofluorescence Assay.
The chlamydia shedding time of LIGHT KO mice was similar to wild type mice, which cleared the organisms within 28 days after primary infection, and acquired protective immunity against C. muridarum reinfection. All mice regardless of genotypes developed severe upper genital tract pathology and showed no significant difference between LIGHT KO and wild type mice. All mice developed robust anti-C. muridarum organism IgG antibody responses and the ratios of IgG2a versus IgG1 showed no significant difference between LIGHT KO and wild type mice. Splenocytes from MoPn-infected LIGHT KO and wild type mice produced high levels of IFN-gamma and IL-17, but IL-4 and IL-5 couldn't be detected.
LIGHT signal pathway may not correlated with protection against C. muridarum urogenital tract infection and urogenital tract pathology induced by C. muridarum.
研究与糖蛋白D竞争疱疹病毒进入T细胞的淋巴毒素样诱导蛋白（LIGHT）在小鼠生殖道衣原体感染期间保护性免疫和病理发展中的作用。
将1×10⁴包涵体形成单位（IFUs）的活鼠衣原体接种到C57BL/6J野生型（wt）和LIGHT缺陷型（LIGHT KO）小鼠的阴道内。每组一半小鼠在初次感染后第49天再次感染。每3或4天采集小鼠阴道拭子以监测活病原体脱落情况。在初次感染后第80天，处死小鼠，分离阴道组织进行病理分析。收集脾细胞，用紫外线灭活的鼠肺炎衣原体（UV-MoPn EB）再次刺激后，通过酶联免疫吸附测定（ELISA）检测脾细胞培养上清液中的白细胞介素-4（IL-4）、白细胞介素-5（IL-5）、白细胞介素-17（IL-17）和干扰素-γ（IFN-γ）。通过间接免疫荧光测定法检测小鼠血清中不同抗体亚型的滴度。
LIGHT KO小鼠的衣原体脱落时间与野生型小鼠相似，在初次感染后28天内清除病原体，并获得了针对鼠衣原体再感染的保护性免疫。所有小鼠，无论基因型如何，均出现严重的上生殖道病理改变，LIGHT KO小鼠和野生型小鼠之间无显著差异。所有小鼠均产生了强烈的抗鼠衣原体IgG抗体反应，LIGHT KO小鼠和野生型小鼠之间IgG2a与IgG1的比例无显著差异。来自感染MoPn的LIGHT KO小鼠和野生型小鼠的脾细胞产生高水平的IFN-γ和IL-17，但未检测到IL-4和IL-5。
LIGHT信号通路可能与抵抗鼠衣原体生殖道感染及鼠衣原体诱导的生殖道病理改变无关。
