AUTHOR=Keck Jonathon , Chambers James P. , Yu Jieh-Juen , Cheng Xingguo , Christenson Lane K. , Guentzel M. N. , Gupta Rishein , Arulanandam Bernard P. 

TITLE=Modulation of Immune Response to Chlamydia muridarum by Host miR-135a

JOURNAL=Frontiers in Cellular and Infection Microbiology

VOLUME=11

YEAR=2021

URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2021.638058

DOI=10.3389/fcimb.2021.638058

ISSN=2235-2988

ABSTRACT=<p>Previously, our laboratory established the role of small, noncoding RNA species<italic>, i.e.</italic>, 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 identified <italic>in silico</italic> to 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 following <italic>Chlamydia muridarum</italic> (Cm) infection. We observed miR-135a regulation of Cm-primed bone marrow derived dendritic cells (BMDC) <italic>via</italic> activation of Cm-immune CD4<sup>+</sup> 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<sup>+</sup> CD4<sup>+</sup> T cells <italic>via</italic> the CXCL10/CXCR3 axis. Collectively, data reported here support miR-135a affecting multiple cellular processes in response to chlamydial infection.</p>