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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: J Immunol. 2015 Aug 3;195(5):2122–2133. doi: 10.4049/jimmunol.1500396

FIGURE 5.

FIGURE 5

CRAC channels regulate generation of inflammatory mediators in response to PAR2 activation in human airway epithelial cells. NHBE cells were stimulated with the PAR2-activating peptide SLIGRL (100 µM) in the absence or presence of BTP2 or following knockdown of both STIM1 and Orai1. Cell-culture supernatants were collected after 2 hours (for PGE2) or 24 hours (for IL-6, IL-8 and GM-CSF measurements) and levels of PGE2, IL-6, IL-8 and GM-CSF were determined by cytokine-specific ELISA kits. (A) PGE2 induction by SLIGRL and Type IX trypsin (100 nM) is inhibited by BTP2 and U73122. A scrambled peptide (LRGILS) and a PAR1-specific peptide (TFLLR) had no effect on PGE2 induction. (B) Inhibition of PGE2 secretion by knockdown of STIM1 and Orai1. (C) Inhibition of IL-6 secretion by BTP2 and (D) siRNA mediated knockdown of STIM1 and Orai1. (E-F) Effect of BTP2 on IL-8 and GM-CSF induction (N=3 replicates, 3 independent experiments).