Pathogenesis of : neutrophilic host response, sustained infection, and clinical sequelaeNeisseria gonorrhoeae: neutrophilic host response, sustained infection, and clinical sequelae in the female reproductive tract: neutrophilic host response, sustained infection, and clinical sequelae

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Abstract

Purpose of review

Gonorrhea is a major global health concern, caused by the bacterium Neisseria gonorrhoeae. The main clinical feature of acute gonorrhea is neutrophilic influx that is unable to clear infection. Women of reproductive age are predominantly at risk for serious sequelae of gonorrhea, including pelvic inflammatory disease, ectopic pregnancy, and infertility. This review will highlight how neutrophils are recruited to the female reproductive tract (FRT) in response to N. gonorrhoeae, how N. gonorrhoeae resists killing by neutrophils, and the connection between neutrophilic inflammation and cellular damage.

Recent findings

Epithelial cells and immune cells of the FRT recognize and respond to N. gonorrhoeae lipid A and heptose bisphosphate of lipooligosaccharide, porin, lipoproteins, and peptidoglycan fragments. N. gonorrhoeae skews the resulting immune response toward a neutrophilic, Th17-like response. N. gonorrhoeae has multiple, nonredundant mechanisms to survive inside neutrophils and in neutrophil extracellular traps. Infection that ascends to the upper FRT induces the further release of inflammatory cytokines and matrix metalloproteinases, which cause epithelial damage.

Summary

N. gonorrhoeae is remarkable in its ability to recruit neutrophils, yet survive in their midst. New models being developed for FRT infection with N. gonorrhoeae will be useful to reveal the mechanisms underlying these observations.

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