Seminar

Pathways of Borrelia burgdorferi-Induced cardiac inflammation

Juan Anguita, PhD

Macrophages play a crucial role in the defense against infectious microorganisms. These phagocytic cells detect pathogens through surface pattern recognition receptors (PRRs), such as Toll- like receptors (TLRs), scavenger receptors (SRs), integrins and lectins. The interaction with PRRs leads to the production of proinflammatory factors, as well as the internalization and degradation of the infecting agent. Cardiac inflammation during infection with the spirochete, Borrelia burgdorferi (the causative agent of Lyme disease) is highly dependent on macrophage function and the balance between their protective phagocytic activity and the resulting proinflammatory cytokine induction. The mechanisms by which macrophages and other phagocytic cells internalize the spirochete are however, largely unknown. We have generated data that show that complement receptor 3 (CR3, Mac-1, CD11b/CD18) is a phagocytic receptor for Bb in murine macrophages. Overall, our data establish CR3 as a MyD88-independent phagocytic receptor for B. burgdorferi that also participates in the modulation of the proinflammatory output of macrophages.