TLR3 deficiency exacerbates the loss of epithelial barrier function during genital tract Chlamydia muridarum infection

BioRxiv : the Preprint Server for Biology
Ramesh KumarWilbert A Derbigny

Abstract

Problem: Chlamydia trachomatis infections are often associated with acute syndromes including cervicitis, urethritis, and endometritis, which can lead to chronic sequalae such as pelvic inflammatory disease (PID), chronic pelvic pain, ectopic pregnancy, and tubal infertility. As epithelial cells are the major cell type productively infected during genital tract Chlamydia infections, we investigated whether Chlamydia has any impact on the integrity of the host epithelial barrier as a possible mechanism to facilitate the dissemination of infection, and examined whether TLR3 function modulates its impact. Method of Study: We used wild-type and TLR3-deficient murine oviduct epithelial (OE) cells to ascertain whether C. muridarum infection had any effect on the epithelial barrier integrity of these cells as measured by transepithelial resistance (TER) and cell permeability assays. We next assessed whether infection impacted the transcription and protein function of the cellular tight-junction (TJ) genes for claudins1-4, ZO-1, JAM1 and occludin via quantitative real-time PCR (qPCR) and western blot. Results: qPCR, immunoblotting, transwell permeability assays, and TER studies show that Chlamydia compromises cellular TJ function throu...Continue Reading

Related Concepts

Acute Disease
Western Blotting
Cell Membrane Permeability
Uterine Cervicitis
Chlamydia Infections
Endometritis
Epithelial Cells
Female Genitalia
Immunoblotting
Mus

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