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• W3154420003 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 identified in silico 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 Chlamydia muridarum (Cm) infection. We observed miR-135a regulation of Cm-primed bone marrow derived dendritic cells (BMDC) via activation 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 cells via the CXCL10/CXCR3 axis. Collectively, data reported here support miR-135a affecting multiple cellular processes in response to chlamydial infection." @default.
• W3154420003 created "2021-04-26" @default.
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• W3154420003 date "2021-04-13" @default.
• W3154420003 modified "2023-09-29" @default.
• W3154420003 title "Modulation of Immune Response to Chlamydia muridarum by Host miR-135a" @default.
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• W3154420003 doi "https://doi.org/10.3389/fcimb.2021.638058" @default.
• W3154420003 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8076868" @default.
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