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Chitinase Induce the Release of IL‐8 in Human Airway Epithelial Cells, Via Ca 2+ ‐dependent PKC and ERK Pathways
Author(s) -
Hong J. Y.,
Lee K. E.,
Kim K. W.,
Sohn M. H.,
Kim K.E.
Publication year - 2010
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2010.02404.x
Subject(s) - chitinase , mapk/erk pathway , protein kinase c , biology , signal transduction , calphostin c , kinase , streptomyces griseus , microbiology and biotechnology , biochemistry , enzyme , streptomyces , genetics , bacteria
Chitinases are produced in significant quantities by hosts defending against infections with chitin‐containing organisms. However, little is known about the immune response of exogenous chitinase in human epithelial cells. IL‐8 has been suggested to have a role in the pathogenesis of the allergenic inflammation of bronchial asthma. We examined whether Streptomyces griseus ( S. griseus ) chitinase‐induced IL‐8 on airway epithelium and identified the involvement of intracellular signalling pathways. H292 cells were treated with S. griseus chitinase with different concentrations and times. The IL‐8 levels were determined by specific human IL‐8 enzyme‐linked immunosorbent assay (ELISA) and reverse transcriptase polymerase chain reaction. Using a series of pharmacological inhibitors, we examined the upstream signalling pathway responsible for IL‐8 expression in response to S. griseus chitinase. Cells exposed to S. griseus chitinase showed higher level of IL‐8 protein production and mRNA expression. Cells stimulated by S. griseus chitinase resulted in the activation of protein kinase C (PKC), extracellular signal‐regulated kinase (ERK) and nuclear factor kappa‐B (NF‐kB) pathways. Inhibitors of Ca 2+ ‐dependent PKC (Ro‐31‐8220, calphostin C and Gő6976) significantly abolished chitinase‐induced expression of IL‐8. However, Ca 2+ ‐independent PKC inhibitor (rottlerin) did not inhibit IL‐8 expression. Through ERK inhibitor (U0126) and NF‐kB inhibitor (caffeine acid phenethyl ester) treatment, it was proven that ERK and NF‐kB regulated chitinase‐induced IL‐8 expression. We concluded that S. griseus chitinase‐induced IL‐8 expression was regulated by the activation of Ca 2± ‐dependent PKC, ERK and NF‐kB in human airway epithelial cells.