Prostaglandin E2-induced interleukin-6 release by a human airway epithelial cell
line.
Tavakoli, S., M. J. Cowan, T. Benfield, C. Logun, and J. H. Shelhamer.
Critical Care Medicine Department, Clinical Center, National Institutes of Health,
Bethesda, Maryland 20892
APStracts 7:0244L, 2000.
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«minus»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«minus»7 to 10«minus»10 M) induced a dose-related increase in
IL-6 release at 24 h. PGF2alpha (10«minus»6 M) treatment caused a similar effect to that
of PGE2 (10«minus»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«minus»6 to 10«minus»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.
Received 6 August 1999; accepted in final form 21 July 2000
APS Manuscript Number L267-9.
Article publication pending Am J Physiol Lung Cell Mol Physiol
ISSN 1080-4757 Copyright 2000 The American Physiological Society.
Published in APStracts on 7 November 2000