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Activation of Ca²⁺-Dependent Signaling by TLR2¹

College of Physicians and Surgeons, Columbia University, New York, NY 10032

Upon contact with airway epithelial cells, bacterial products activate Ca²⁺ fluxes that are required for induction of NF-B-dependent gene expression. TLR2 is apically displayed on airway cells, making it a likely transducer linking bacterial stimuli and kinases that affect Ca²⁺ release. Using biochemical and genetic approaches, we demonstrate that TLR2 ligands stimulate release of Ca²⁺ from intracellular stores by activating TLR2 phosphorylation by c-Src, and recruiting PI3K and phospholipase C to affect Ca²⁺ release through inositol (1,4,5) trisphosphate receptors. In the absence of TLR2, murine macrophages as well as airway cells do not generate Ca²⁺ fluxes or induce proinflammatory signaling. Thus, Ca²⁺ participates as a second messenger in TLR2-dependent signaling and provides another target to modulate proinflammatory responses to bacterial infection.

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