Figure 5.

Host response to A. actinomycetemcomitans infection in the mouth. Interaction between bacterial cells and gingival tissue causes the release of cytokine signals by lymphocytes and other WBCs. Cytokine signaling results in the activation of circulating WBCs in the underlying vasculature. Activation results in the immunological priming of WBCs and a conformational change of LFA-1 from a low-affinity state to a high-affinity, exposed state. High-affinity, activated LFA-1 can bind ICAM-1 expressed by vascular endothelial cells. Interaction between ICAM-1 and LFA-1 results in the migration of WBCs into the infected tissue via the process of diapedesis. In the gingival tissue, WBCs are incapacitated by secreted LtxA binding to activated LFA-1, allowing A. actinomycetemcomitans to colonize, persist, and invade deeper into the periodontal pocket.