Open AccessInterleukin-17 Contributes to Generation of Th1 Immunity and Neutrophil Recruitment duringChlamydia muridarumGenital Tract Infection but Is Not Required for Macrophage Influx or Normal Resolution of Infection
Author(s) -
Amy M. Scurlock,
Lauren C. Frazer,
Charles W. Andrews,
Catherine M. O’Connell,
Isaac P. Foote,
Sarabeth L. Bailey,
Kumar Chandra-Kuntal,
Jay K. Kolls,
Toni Darville
Publication year - 2011
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.00984-10
Subject(s) - chlamydia , biology , immunology , immunity , macrophage , tumor necrosis factor alpha , immune system , genital tract , sex organ , inflammation , cellular immunity , in vitro , physiology , biochemistry , genetics
Interleukin 17 (IL-17) contributes to development of Th1 immunity and neutrophil influx duringChlamydia muridarum pulmonary infection, but its role duringC. muridarum genital tract infection has not been described. We detected similar numbers ofChlamydia -specific Th17 and Th1 cells in iliac nodes of wild-type mice early during genitalC. muridarum infection, while Th1 cells predominated later.il17ra − / − mice exhibited a reduced chlamydia-specific Th1 response in draining iliac nodes and decreased local IFN-γ production. Neutrophil influx into the genital tract was also decreased. However,il17ra − / − mice resolved infection normally, and no difference in pathology was observed compared to the wild type. Macrophage influx and tumor necrosis factor alpha (TNF-α) production were increased inil17ra − / − mice, providing a compensatory mechanism to effectively control chlamydial genital tract infection despite a reduced Th1 response. Inifn γ− / − mice, a marked increase in cellular infiltrates and chronic pathology was associated with an increased Th17 response. Although neutralization of IL-17 inifn γ− / − 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 ofC. muridarum 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.