The chronic inflammatory disease periodontitis results from disruption of homeostasis between the peri-odontal tissue and the microbiota. Bone loss and tissue damage are consequences of excessive host inflammation, in which TLRs and complement have been implicated. Additionally, the periodontal pathogen Porphyromonas gingivalis can subvert the C5a receptor (C5aR) during the initiation of disease. Abe et al. (p. 5442) therefore investigated the involvement of C5aR in periodontitis pathogenesis and its potential as a therapeutic target. Because mice lacking either C5aR or TLR2 are resistant to periodontitis, and complement activation can synergize with TLR signaling, the authors assayed for C5aR—TLR2 synergy in periodontitis. Indeed, activation of C5aR and TLR2 synergistically enhanced inflammatory cy-tokine production in the gingiva, compared with activation of either receptor alone.
展开▼
