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Published online before print June 3, 2003

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© 2003 by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1102571

Received for publication November 19, 2002.
Revised March 16, 2003.
Accepted for publication March 17, 2003.

Article

IL-4 primes human endothelial cells for secondary responses to histamine

Tom Wierzbicki ^*, Shehzad M. Iqbal , Susan L. Cuvelier , Geneve Awong , Lee Anne Tibbles , and Kamala D. Patel ^*@

Departments ofPhysiology and Biophysics and *Biochemistry and Molecular Biology. Immunology Research Group, University of Calgary, Alberta, Canada

^@ To whom correspondence should be addressed. E-mail: kpatel{at}ucalgary.ca.

	Abstract

Interleukin-4 (IL-4) is a multifunctional cytokine, which is involved in numerous disease states, including atopic asthma. IL-4 not only induces direct responses in cells but can also prime for secondary responses to stimuli. Little is known about the priming effects of IL-4 on endothelial cells; therefore, we chose to examine the ability of IL-4 to prime endothelial cells for platelet-activating factor (PAF) synthesis and prostaglandin E₂ (PGE₂) release. IL-4 alone did not enhance PAF synthesis or PGE₂ release; however, pretreatment with IL-4 primed for PAF synthesis and PGE₂ release in response to subsequent stimulation with histamine. In contrast, tumor necrosis factor , oncostatin M, and IL-1 did not prime endothelial cells for PAF synthesis in response to histamine. The priming effects of IL-4 occurred without any detectable changes in the requirement for signaling pathways upstream of PGE₂ release. IL-4 treatment increased the expression of mRNA for histamine receptor 1 (HR1) and shifted the inhibition cure for pyrilamine, a specific HR1 antagonist. In addition, the dose-response curve for histamine-induced elevations in intracellular calcium was shifted following IL-4 stimulation. Together, these data indicate that HR1 is up-regulated in IL-4-stimulated human umbilical vein endothelial cell (HUVEC) and suggest that this up-regulation may contribute to the enhanced responsiveness of IL-4-stimulated HUVEC to histamine.

Key Words: G protein-coupled receptor • HUVEC • platelet-activating factor • prostaglandin E₂

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