The focus of our group is to elucidate how the complement system (an arm of innate immune defenses) interacts with Neisseria gonorrhoeae (the bacteria that cause gonorrhea) and N. meningitidis (the agent of bacterial meningitis). This knowledge is now being used to develop novel immunotherapeutics and vaccines against multidrug-resistant gonorrhea. Gonococci scavenge host complement inhibitors to escape killing by complement. The first approach being investigated includes fusing the microbial binding region of complement inhibitors with the Fc region of antibody, which enhances complement-dependent lysis of bacteria. A key aspect of gonococcal pathogenesis is its ability to use a sugar called sialic acid from the host to escape immune defenses. In the second approach, we are investigating the use of analogs of sialic acid that are taken up by the bacteria, but unlike the ‘physiological’ form of sialic acid, fail to protect the bacteria against host defenses and results in faster clearance of bacteria in the murine model of gonorrhea. In collaboration with Dr. Peter Rice's group at UMass, our group is developing a monoclonal antibody and a vaccine that target a gonococcal glycan epitope.