Modulation of Immune Response to Chlamydia muridarum by Host miR-135a
Abstract
Previously, our laboratory established the role of small, noncoding RNA species, i.e., microRNA (miRNA) including miR-135a in anti-chlamydial immunity in infected hosts. We report here chlamydial infection results in decreased miR-135a expression in mouse genital tissue and a fibroblast cell line. Several chemokine and chemokine receptor genes (including CXCL10, CCR5) associated with chlamydial pathogenesis were identifiedin silicoto contain putative miR-135a binding sequence(s) in the 3’ untranslated region. The role of miR-135a in the host immune response was investigated using exogenous miR-135a mimic to restore the immune phenotype associated with decreased miR-135a followingChlamydia muridarum(Cm) infection. We observed miR-135a regulation of Cm-primed bone marrow derived dendritic cells (BMDC)viaactivation of Cm-immune CD4+T cells for clonal expansion and CCR5 expression. Using a transwell cell migration assay, we explore the role of miR-135a in regulation of genital tract CXCL10 expression and recruitment of CXCR3+CD4+T cellsviathe CXCL10/CXCR3 axis. Collectively, data reported here support miR-135a affecting multiple cellular processes in response to chlamydial infection.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 13, 2021
- Source ID
- 10.3389/fcimb.2021.638058
Entities
People
- Bernard P Arulanandam
- James P. Chambers
- Jieh-Juen Yu
- Jonathon Keck
- Lane K. Christenson
- M. N. Guentzel
- Rishein Gupta
- Xingguo Cheng
Organizations
- Army Research Office