Bacteria modulate host-cell responses by capitalizing on the lipid raft structure

Evaluation of: Hajishengallis G, Wang M, Liang S, Triantafilou M, Triantafilou K: Pathogen induction of CXCR4/TLR2 cross-talk impairs host defense function. PNAS 105 (36), 13532-13537 (2008). Bacterial modulation of the innate host response is a rapidly evolving field. From bacterial effector proteins secreted into host cells to lipopolysaccharide lipid A structures that block Toll-like receptor function, we are learning that bacterial pathogenesis often involves downregulation of innate host responses. In the report by Hajishengallis et al. we learn that Porphyromonas gingivalis capitalizes on the lipid raft structure to downmodulate innate defense mechanisms. Remarkably, this novel mechanism employs host-cell signaling pathways through cross-talk between Toll-like receptor-2/chemokine receptor 4 to attenuate the protective and bactericidal response to P. gingivalis infection. This subtle subversion of host signaling may contribute to the chronic and persistent nature of P. gingivalis-associated diseases.