Chlamydia muridarum infection associated host MicroRNAs in the murine genital tract and contribution to generation of host immune response.

Chlamydia muridarum infection associated host MicroRNAs in the murine genital tract and contribution to generation of host immune response.
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衣原体墨陀感染与鼠生生殖道中的宿主microRNA相关联,并对产生宿主免疫反应的贡献。

DOI:
10.1111/aji.12281
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发表时间:
2015-02
期刊:
American journal of reproductive immunology (New York, N.Y. : 1989)
影响因子:
--
通讯作者:
Arulanandam BP
Arulanandam BP
中科院分区:
其他
文献类型:
--
作者:
Gupta R;Arkatkar T;Yu JJ;Wali S;Haskins WE;Chambers JP;Murthy AK;Bakar SA;Guentzel MN;Arulanandam BP

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沙眼衣原体(CT)是人类主要的性传播细菌感染,与生殖道损伤有关。然而,人们对微小RNA(miRs)在生殖器CT中的参与和调节知之甚少。我们分析了C.小鼠(CT的鼠品系)攻击,以及攻击后第6天和第12天的CD 4 + T细胞缺陷型(CD 4-/-)C57 BL/6小鼠。在第6天,在较低GT中显著下调的miR是miR-125 b-5 p、−16、−214、− 23 b、− 135 a、−182、−183、− 30 c和− 30 e,而−146和−451显著上调,在细菌挑战后第12天未显示出特征。在C中观察到miR-125 b-5 p(+5.06倍变化),− 135 a(+4.9),−183(+7.9)和−182(+3.2)的显著差异。与WT小鼠相比,小鼠感染了CD 4 −/−。计算机模拟预测和质谱分析揭示了miR-135 a和-182及其相关蛋白(即热休克蛋白B1和α-2HS-糖蛋白)的调控。这项研究提供了生殖器衣原体感染后miR调节的证据,表明其在发病机制和宿主免疫中的作用。
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 i.e, 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.
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