{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,6]],"date-time":"2026-05-06T01:53:39Z","timestamp":1778032419987,"version":"3.51.4"},"reference-count":47,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2011,3,1]],"date-time":"2011-03-01T00:00:00Z","timestamp":1298937600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2011,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Interleukin 17 (IL-17) contributes to development of Th1 immunity and neutrophil influx during<jats:italic>Chlamydia muridarum<\/jats:italic>pulmonary infection, but its role during<jats:italic>C. muridarum<\/jats:italic>genital tract infection has not been described. We detected similar numbers of<jats:italic>Chlamydia<\/jats:italic>-specific Th17 and Th1 cells in iliac nodes of wild-type mice early during genital<jats:italic>C. muridarum<\/jats:italic>infection, while Th1 cells predominated later.<jats:italic>il17ra<\/jats:italic><jats:sup>\u2212<\/jats:sup><jats:sup><jats:italic>\/<\/jats:italic><\/jats:sup><jats:sup>\u2212<\/jats:sup>mice exhibited a reduced chlamydia-specific Th1 response in draining iliac nodes and decreased local IFN-\u03b3 production. Neutrophil influx into the genital tract was also decreased. However,<jats:italic>il17ra<\/jats:italic><jats:sup>\u2212<\/jats:sup><jats:sup><jats:italic>\/<\/jats:italic><\/jats:sup><jats:sup>\u2212<\/jats:sup>mice resolved infection normally, and no difference in pathology was observed compared to the wild type. Macrophage influx and tumor necrosis factor alpha (TNF-\u03b1) production were increased in<jats:italic>il17ra<\/jats:italic><jats:sup>\u2212<\/jats:sup><jats:sup><jats:italic>\/<\/jats:italic><\/jats:sup><jats:sup>\u2212<\/jats:sup>mice, providing a compensatory mechanism to effectively control chlamydial genital tract infection despite a reduced Th1 response. In<jats:italic>ifn<\/jats:italic>\u03b3<jats:sup>\u2212<\/jats:sup><jats:sup><jats:italic>\/<\/jats:italic><\/jats:sup><jats:sup>\u2212<\/jats:sup>mice, a marked increase in cellular infiltrates and chronic pathology was associated with an increased Th17 response. Although neutralization of IL-17 in<jats:italic>ifn<\/jats:italic>\u03b3<jats:sup>\u2212<\/jats:sup><jats:sup><jats:italic>\/<\/jats:italic><\/jats:sup><jats:sup>\u2212<\/jats:sup>mice decreased neutrophil influx, macrophage infiltration remained intact and the bacterial burden was not increased. Collectively, these results indicate that IL-17 contributes to the generation of Th1 immunity and neutrophil recruitment but is not required for macrophage influx or normal resolution of<jats:italic>C. muridarum<\/jats:italic>genital infection. These data highlight the redundant immune mechanisms operative at this mucosal site and the importance of examining site-specific responses to mucosal pathogens.<\/jats:p>","DOI":"10.1128\/iai.00984-10","type":"journal-article","created":{"date-parts":[[2010,12,14]],"date-time":"2010-12-14T04:43:35Z","timestamp":1292301815000},"page":"1349-1362","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":107,"title":["Interleukin-17 Contributes to Generation of Th1 Immunity and Neutrophil Recruitment during<i>Chlamydia muridarum<\/i>Genital Tract Infection but Is Not Required for Macrophage Influx or Normal Resolution of Infection"],"prefix":"10.1128","volume":"79","author":[{"given":"Amy M.","family":"Scurlock","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute, 13 Children's Way, Slot 512-13, Little Rock, Arkansas 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