| First Author | Gyorke CE | Year | 2020 |
| Journal | J Immunol | Volume | 205 |
| Issue | 11 | Pages | 3037-3049 |
| PubMed ID | 33087404 | Mgi Jnum | J:300716 |
| Mgi Id | MGI:6502524 | Doi | 10.4049/jimmunol.2000600 |
| Citation | Gyorke CE, et al. (2020) IL-1alpha Is Essential for Oviduct Pathology during Genital Chlamydial Infection in Mice. J Immunol 205(11):3037-3049 |
| abstractText | Chlamydia trachomatis infection of the female genital tract can lead to irreversible fallopian tube scarring. In the mouse model of genital infection using Chlamydia muridarum, IL-1R signaling plays a critical role in oviduct tissue damage. In this study, we investigated the pathologic role of IL-1alpha, one of the two proinflammatory cytokines that bind to IL-1R. Il1a(-/-) mice infected with C. muridarum cleared infection at their cervix at the same rate as wild-type (WT) mice, but were significantly protected from end point oviduct damage and fibrosis. The contribution of IL-1alpha to oviduct pathology was more dramatic than observed in mice deficient for IL-1beta. Although chlamydial burden was similar in WT and Il1a(-/-) oviduct during peak days of infection, levels of IL-1beta, IL-6, CSF3, and CXCL2 were reduced in Il1a(-/-) oviduct lysates. During infection, Il1a(-/-) oviducts and uterine horns exhibited reduced neutrophil infiltration, and this reduction persisted after the infection resolved. The absence of IL-1alpha did not compromise CD4 T cell recruitment or function during primary or secondary chlamydial infection. IL-1alpha is expressed predominantly by luminal cells of the genital tract in response to infection, and low levels of expression persisted after the infection cleared. Ab-mediated depletion of IL-1alpha in WT mice prevented infection-induced oviduct damage, further supporting a key role for IL-1alpha in oviduct pathology. |
