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Am J Physiol Lung Cell Mol Physiol 280: L127-L133, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 1, L127-L133, January 2001

Prostaglandin E2-induced interleukin-6 release by a human airway epithelial cell line

S. Tavakoli, M. J. Cowan, T. Benfield, C. Logun, and J. H. Shelhamer

Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892

Human airway epithelial cell release of interleukin (IL)-6 in response to lipid mediators was studied in an airway cell line (BEAS-2B). Prostaglandin (PG) E2 (10-7 M) treatment caused an increase in IL-6 release at 2, 4, 8, and 24 h. IL-6 release into the culture medium at 24 h was 3,396 ± 306 vs. 1,051 ± 154 pg/ml (PGE2-treated cells vs. control cells). PGE2 (10-7 to 10-10 M) induced a dose-related increase in IL-6 release at 24 h. PGF2alpha (10-6 M) treatment caused a similar effect to that of PGE2 (10-7 M). PGE2 analogs with relative selectivity for PGE2 receptor subtypes were studied. Sulprostone, a selective agonist for the EP-3 receptor subtype had no effect on IL-6 release. 11-Deoxy-16,16-dimethyl-PGE2, an EP-2/4 agonist, and 17-phenyl trinor PGE2, an agonist selective for the EP-1 > EP-3 receptor subtype (10-6 to 10-8 M), caused dose-dependent increases in IL-6 release. 8-Bromo-cAMP treatment resulted in dose-related increases in IL-6 release. RT-PCR of BEAS-2B cell mRNA demonstrated mRNA for EP-1, EP-2, and EP-4 receptors. After PGE2 treatment, increases in IL-6 mRNA were noted at 4 and 18 h. Therefore, PGE2 increases airway epithelial cell IL-6 production and release.

cytokines; eicosanoids; lung inflammation


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