Open AccessType I Interferon Signaling Exacerbates Chlamydia muridarum Genital Infection in a Murine Model
Author(s) -
Uma M. Nagarajan,
Daniel Prantner,
James D. Sikes,
Charles W. Andrews,
Anna Goodwin,
Shanmugam Nagarajan,
Toni Darville
Publication year - 2008
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00629-08
Subject(s) - biology , chlamydia , immunology , interferon , chlamydiaceae , sex organ , virology , interferon type i , genetics
Type I interferons (IFNs) induced during in vitro chlamydial infection exert bactericidal and immunomodulatory functions. To determine the precise role of type I IFNs during in vivo chlamydial genital infection, we examined the course and outcome ofChlamydia muridarum genital infection in mice genetically deficient in the receptor for type I IFNs (IFNAR−/− mice). A significant reduction in chlamydial shedding and duration of lower genital tract infection was observed in IFNAR−/− mice in comparison to the level of chlamydial shedding and duration of infection in wild-type (WT) mice. Furthermore, IFNAR−/− mice developed less chronic oviduct pathology in comparison to that in WT mice. Compared to the WT, IFNAR−/− mice had a greater number of chlamydial-specific T cells in their iliac lymph nodes 21 days postinfection. IFNAR−/− mice also exhibited earlier and enhanced CD4 T-cell recruitment to the cervical tissues, which was associated with increased expression of CXCL9 in the genital secretions of IFNAR−/− mice, but not with expression of CXCL10, which was reduced in the genital secretions of IFNAR−/− mice. These data suggest that type I IFNs exacerbateC. muridarum genital infection through an inhibition of the chlamydial-specific CD4 T-cell response.