The role of complement receptor 3(CR3) in Neisseria gonorrhoeae infection of human cervical epithelia

Neisseria gonorrhoeae is an important sexually transmitted pathogen and a m ajor cofactor in HIV-1 infection. This organism uses different mechanisms t o infect male and female genital tract epithelia. Receptor-mediated endocyt osis of N. gonorrhoeae is the principle mechanism of entry into male urethr al epithelial cells. Infection in men leads to a pronounced inflammatory re sponse. In contrast, N. gonorrhoeae infection in women induces ruffling of the cervical epithelia, allowing a macropinocytic mechanism of entry. Infec tion in women is frequently asymptomatic, suggesting suppression of the inf lammatory response. N. gonorrhoeae-induced membrane ruffling and inflammati on suppression are consistent with the ability of this bacterium to enter c ervical epithelial cells, in vitro and in vivo, by interaction with complem ent receptor 3 (CR3), a receptor that does not trigger an inflammatory resp onse. This receptor is present on cervical epithelial cells but not on male urogenital tract epithelia. N. gonorrhoeae engagement of CR3 initiates a u nique mechanism of bacterial-induced membrane ruffling and internalization. These studies explain why the pathology of N. gonorrhoeae infection differ s between males and females. Additionally, the observation that this recept or is present on cervical epithelia may provide insight into the pathogenes is of other sexually transmitted pathogens.