Gupta Rishein, Arkatkar Tanvi, Yu Jieh-Juen, Wali Shradha, Haskins William E, Chambers James P, Murthy Ashlesh K, Bakar Sazaly Abu, Guentzel M Neal, Arulanandam Bernard P
South Texas Center for Emerging Infectious Diseases and Center of Excellence in Infection Genomics, University of Texas at San Antonio, San Antonio, TX, USA.
Am J Reprod Immunol. 2015 Feb;73(2):126-40. doi: 10.1111/aji.12281. Epub 2014 Jun 28.
Chlamydia trachomatis (CT) is the leading sexually transmitted bacterial infection in humans and is associated with reproductive tract damage. However, little is known about the involvement and regulation of microRNAs (miRs) in genital CT.
We analyzed miRs in the genital tract (GT) following C. muridarum (murine strain of CT) challenge of wild type (WT) and CD4(+) T-cell deficient (CD4(-/-)) C57BL/6 mice at days 6 and 12 post-challenge.
At day 6, miRs significantly downregulated in the lower GT were miR-125b-5p, -16, -214, -23b, -135a, -182, -183, -30c, and -30e while -146 and -451 were significantly upregulated, profiles not exhibited at day 12 post-bacterial challenge. Significant differences in miR-125b-5p (+5.06-fold change), -135a (+4.9), -183 (+7.9), and -182 (+3.2) were observed in C. muridarum-infected CD4(-/-) compared to WT mice. In silico prediction and mass spectrometry revealed regulation of miR-135a and -182 and associated proteins, that is, heat-shock protein B1 and alpha-2HS-glycoprotein.
This study provides evidence on regulation of miRs following genital chlamydial infection suggesting a role in pathogenesis and host immunity.
沙眼衣原体（CT）是人类主要的性传播细菌感染病原体，与生殖道损伤有关。然而，关于微小RNA（miR）在生殖道沙眼衣原体感染中的作用及调控机制知之甚少。
我们在野生型（WT）和CD4(+) T细胞缺陷型（CD4(-/-)）C57BL/6小鼠感染鼠沙眼衣原体（CT的鼠株）后第6天和第12天，分析其生殖道中的miR。
在第6天，下生殖道中显著下调的miR有miR-125b-5p、-16、-214、-23b、-135a、-182、-183、-30c和-30e，而-146和-451显著上调，这些表达谱在细菌感染后第12天未出现。与WT小鼠相比，在感染鼠沙眼衣原体的CD4(-/-)小鼠中观察到miR-125b-5p（变化倍数为+5.06）、-135a（+4.9）、-183（+7.9）和-182（+3.2）有显著差异。计算机模拟预测和质谱分析揭示了miR-135a和-182及其相关蛋白（即热休克蛋白B1和α-2HS-糖蛋白）的调控情况。
本研究提供了生殖道衣原体感染后miR调控的证据，提示其在发病机制和宿主免疫中发挥作用。
