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Infection and Immunity, October 2008, p. 4642-4648, Vol. 76, No. 10
0019-9567/08/$08.00+0     doi:10.1128/IAI.00629-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Type I Interferon Signaling Exacerbates Chlamydia muridarum Genital Infection in a Murine Model{triangledown}

Uma M. Nagarajan,1* Daniel Prantner,2 James D. Sikes,1 Charles W. Andrews Jr.,3 Anna M. Goodwin,1 Shanmugam Nagarajan,2 and Toni Darville1,{dagger}

Division of Pediatric Infectious Diseases, Arkansas Children's Hospital Research Institute, Little Rock, Arkansas 72202,1 Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205,2 Department of Pathology, Rockdale Medical Center, Conyers, Georgia 300123

Received 22 May 2008/ Returned for modification 26 June 2008/ Accepted 18 July 2008

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 of Chlamydia 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 exacerbate C. muridarum genital infection through an inhibition of the chlamydial-specific CD4 T-cell response.

* Corresponding author. Mailing address: Division of Pediatric Infectious Diseases, Arkansas Children's Hospital Research Institute, 1120 Marshall Street, Room 2052, Little Rock, AR 72202. Phone: (501) 364-2479. Fax: (501) 364-2403. E-mail: nagarajanuma{at}uams.edu

{triangledown} Published ahead of print on 28 July 2008.

Editor: B. A. McCormick

{dagger} Present address: Department of Pediatrics, University of Pittsburgh Medical Center, Pittsburgh, PA 15213.

Infection and Immunity, October 2008, p. 4642-4648, Vol. 76, No. 10
0019-9567/08/$08.00+0     doi:10.1128/IAI.00629-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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