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To survive in macrophages,  Coxiella burnetii  hijacks the activation pathway of macrophages. Recently, we have demonstrated that  C. burnetii , via its lipopolysaccharide (LPS), avoids the activation of p38α-MAPK through an antagonistic engagement of Toll-like receptor (TLR)-4. We investigated the fine-tuned mechanism leading to the absence of activation of the p38α-MAPK despite TLR-4 engagement. In macrophages challenged with LPS from the avirulent variants of  C. burnetii , TLR-4 and TLR-2 co-immunoprecipitated. This association was absent in cells challenged by the LPS of pathogenic  C. burnetii . The disruption makes TLRs unable to signal during the recognition of the LPS of pathogenic  C. burnetii . The disruption of TLR-2 and TLR-4 was induced by the re-organization of the macrophage cytoskeleton by  C. burnetii  LPS. Interestingly, blocking the actin cytoskeleton re-organization relieved the disruption of the association TLR-2/TLR-4 by pathogenic  C. burnetii  and rescued the p38α-MAPK activation by  C. burnetii . We elucidated an unexpected mechanism allowing pathogenic  C. burnetii  to avoid macrophage activation by the disruption of the TLR-2 and TLR-4 association.

Coxiella burnetii lipopolysaccharide blocks p38Î±-MAPK activation through the disruption of TLR-2 and TLR-4 association