Cellular Mechanisms Involved in Host Responses to Recombinant HagB of Porphyromonas gingivalis

Objectives:Porphyromonas gingivalis a black-pigmented, anaerobic, gram-negative bacterium has been implicated as a major etiologic agent in the development of human adult periodontitis, a chronic inflammatory process characterized by the destruction of the supportive tissues surrounding teeth. In recent years, associations have also been made between periodontal pathogens like P. gingivalis and cardiovascular disease and low birth weight babies. Therefore, understanding the mechanisms involved in the pathogenesis of periodontitis and the development of measures to prevent or limit this disease process will help in improving the overall health of the host. P. gingivalis possess a variety of virulence factors such as the non-fimbrial adhesin, hemagglutinin B that is thought to be involved in the adherence of the pathogen to host tissues. Methods:We have previously shown that systemic immunization with recombinant HagB (rHagB) results in the induction of an immune response protective against P. gingivalis infection. Results:However, the cellular mechanisms involved in the regulation of host responses to rHagB are not completely understood. Conclusions:Recently, we have demonstrated the involvement of the B7 costimulatory molecules, especially B7-2 (CD86) in specific anti-HagB responses. Furthermore, the cell signaling pathways involved in host responses to rHagB include the kinases ERK 1/2, JNK and p38, as well as NF-ƒÛB transcription factor.Supported by USPHS grants DE 09081 and DE 14215.