The incidence of gonorrhea continues at epidemic levels and at a substantial health care cost both to the individual and the nation. Control of this disease can only be accomplished through adequate, effective immunoprophylaxsis. This vaccine should be directed at inhibiting specifi functions used by the gonococcus to invade the human host. The function of gonococcal pili and the role these molecules play in adhering gonococci to human cells is well understood. However, knowledge of the subsequent invasion process and how gonococci invade human tissues is unclear. The components of the gonococcus responsible for this action would be prime candidates for an effective gonococcal vaccine. Our studies have shown that the porin (protein I) may mediate this invasion mechanism by being transferred from the bacterial membrane to host cell membranes. This event would open aqueous channels within the human cells and change their membrane potential. This may mimic the host cell signal to begin phagocytosis. We would like to examine the molecular details of this event. We will find out if this event occurs in relevant biological membranes. We will measure the membrane potential change caused by this event and what ions are responsible. The membrane fluidity parameters which are important will be defined. We will also examine if protein I has any direction action on the hosts's cellular control mechanisms. We would like to understand the possible lectin-like properties of the gonococcal heat-modifiable proteins II. Once we understand the ligands that are involved in this process, it will be clearer whether or not these proteins influence the transfer of protein I into host cells.
