Infection of the genital tract with Neisseria gonorrhoeae is typically associated with an influx of neutrophils, but the mechanisms underlying this influx are not well understood. The importance of the newly defined lineage of Th17 cells in inflammatory immune responses to infection, including the recruitment of neutrophils, has become increasingly recognized. We have previously shown that N. gonorrhoeae elicits production of IL-17 and other Th17-associated cytokines in vitro and hypothesized that IL-17 plays a role in the induction of chemokines and cytokines which lead to the recruitment of neutrophils to the site of infection. We tested this using a mouse vaginal gonococcal infection model to compare neutrophil recruitment in wild type and IL-17 receptor (IL-17R) knockout mice. The IL-17RKO mice were severely deficient in recruitment of neutrophils to the genital tract. Mouse genital explants were incubated ex vivo with either N. gonorrhoeae or a control antigen and assayed for production of cytokines and chemokines. Genital explants from IL-17RKO mice incubated with N. gonorrhoeae showed decreased production of IL-6 and the neutrophil-attractant chemokines LIX and MIP2α compared to those from wild type mice. These results indicate that N. gonorrhoeae elicits a Th17 response which drives the production of neutrophil-attractant chemokines, resulting in the influx of neutrophils into the genital tract.