| First Author | Nagarajan UM | Year | 2008 |
| Journal | Infect Immun | Volume | 76 |
| Issue | 10 | Pages | 4642-8 |
| PubMed ID | 18663004 | Mgi Jnum | J:140222 |
| Mgi Id | MGI:3812288 | Doi | 10.1128/IAI.00629-08 |
| Citation | Nagarajan UM, et al. (2008) Type I interferon signaling exacerbates Chlamydia muridarum genital infection in a murine model. Infect Immun 76(10):4642-8 |
| abstractText | 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. |
