Title: 512 The Transient Receptor Potential (Trp) Ion Channels TRPA1 and TRPV4 Mediate Inflammatory Pain in the Pancreas
Abstract: cultured as polarized model epithelium.Flow cytometric analyses were used to determine cellular proliferation and F-actin accumulation.CCR6 expression and activation of motogenic signaling pathways were defined using immunoblot and immunofluorescence microscopy analyses.Results: CaCo2 and IEC-6 intestinal cell lines express CCR6 congruent with data from human colonic epithelium.HBD2 was equally potent as the CCR6 cognate ligand CCL20 and control TGFbeta in stimulating migration of wounded epithelial monolayers.Consistent with epithelial restitution, HBD2 and CCL20 did not induce proliferation.Neutralizing antibody to CCR6 markedly decreased HBD2 and CCL20-induced migration, specifying a role for that receptor in IEC6 and CaCo2 epithelial wound healing.HBD2 and CCL20 stimulated an increase in intracellular calcium, phosphorylation of myosin light chain, and accumulation of F-actin.HBD2 and CCL20 were unable to rescue migration blocked by Rho-kinase inhibition, together indicating that CCR6 activates canonical wound healing mechanisms.Conclusions: CCR6-mediated restitution further expands the mechanistic role for chemokines in mucosal inflammation to include wound healing responses in addition to the well-characterized trafficking of immunocytes.These exciting data demonstrate that HBD2 has dual benefits as a frontline defense molecule through the concomitant killing of microbes and activation of restitutive migration to limit entry of noxious stimuli.
Publication Year: 2008
Publication Date: 2008-04-01
Language: en
Type: article
Indexed In: ['crossref']
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Cited By Count: 2
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