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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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