Neisseria gonorrhoeae (Gc) is a sexually transmitted infectious agent that is the only causative agent of the disease gonorrhea. As a strict human pathogen, this bacterium has evolved sophisticated mechanisms to facilitate colonization and growth within affected human populations and its spread. Central to the disease gonorrhea is the massive influx of white cells that occurs in both males and females during symptomatic Gc infection. This "purulent exudate" consists predominately of human polymorphonuclear lymphocytes (PMNs) with associated viable Gc. The interplay between Gc and the PMN is an essential part of pathogenesis. This competitive renewal will continue to explore the molecular mechanisms used by novel factors we have identified that are important for the interaction of Gc and PMNs, to uncover new mechanisms important for Gc survival within and among PMNs, and to determine how Gc modulates the apoptotic pathways of PMNs.
Neisseria gonorrhoeae causes the disease gonorrhea and survives and modulates the anti- microbial actions of human polymorphonuclear lymphocytes (PMNs). This work will uncover new virulence factors important for N. gonorrhoeae survival within and among PMNs,and to determine how N. gonorrhoeae modulates PMN function.
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