Chlamydia muridarum Infection Associated Host MicroRNAs in the Murine Genital Tract and Contribution to Generation of Host Immune Response
Version of Record online: 28 JUN 2014
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
American Journal of Reproductive Immunology
Volume 73, Issue 2, pages 126–140, February 2015
How to Cite
Chlamydia muridarum infection associated host MicroRNAs in the murine genital tract and contribution to generation of host immune response. Am J Reprod Immunol 2015; 73: 126–140, , , , , , , , , .
- Issue online: 12 JAN 2015
- Version of Record online: 28 JUN 2014
- Manuscript Accepted: 21 MAY 2014
- Manuscript Received: 13 FEB 2014
- National Institutes of Health. Grant Number: 1RO1AI074860
- Army Research Office of the Department of Defense. Grant Number: W911NF-11-1-0136
- Chlamydia muridarum ;
- host responses;
- murine genital tract
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.