American journal of reproductive immunology (New York, N.Y. : 1989) · 2014
Chlamydia muridarum infection associated host MicroRNAs in the murine genital tract and contribution to generation of host immune response.
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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
Аннотация
PROBLEM: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: This study provides evidence on regulation of miRs following genital chlamydial infection suggesting a role in pathogenesis and host immunity.
METHODS: 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.
RESULTS: 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.
CONCLUSION: This study provides evidence on regulation of miRs following genital chlamydial infection suggesting a role in pathogenesis and host immunity.