HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tauber, A. I. Articles by Austen, K. F. Search for Related Content PubMed Articles by Tauber, A. I. Articles by Austen, K. F.

Immunologic Release of Histamine and Slow Reacting Substance of Anaphylaxis from Human Lung

V. Effects of Prostaglandins on Release of Histamine¹

From the Departments of Medicine, Harvard Medical School and the Robert B. Brigham Hospital, Boston, Massachusetts 02120

Abstract

The capacity of prostaglandins to suppress the IgE-dependent antigen-induced release of histamine from human lung tissue requires concentrations which increase tissue levels of cyclic adenosine 3',5'-monophosphate (cyclic AMP) and involves a receptor distinct from that utilized by beta adrenergic agents. The inhibition of histamine release and concomitant rise of cyclic AMP in response to prostaglandin E₁ (PGE₁) occurs in a dose response fashion, reaching a peak within 1 min and persisting for at least 60 min. That the supression of mediator release from the subpopulation of target cells by the prostaglandins is related to elevations in total tissue cyclic AMP is supported by the kinetic relationship of the two events, the augmentation of both events in the presence of a methylxanthine, and the finding that the relative potency of isoproterenol, norepinephrine, PGE₁ and prostaglandin F₂ (PGF₂) to inhibit mediator release is in accord with their relative capacity to elevate cyclic AMP. The finding that low doses of prostaglandins enhance mediator release while reducing tissue levels of cyclic AMP reveals that these agents could profoundly modulate the immunologic release of chemical mediators.

Footnotes

¹ This work was supported by Grants AI-07722, AI-10356, and RR-05669 from the National Institutes of Health and a grant from the John A. Hartford Foundation, Inc.

² Fourth-year medical student, Tufts University School of Medicine, Boston, Massachusetts.

³ Postdoctoral trainee supported by The American Thoracic Society.

⁴ Recipient of Research Career Development Award AI-28405 from the National Institutes of Health.

This article has been cited by other articles:

				T. V. HARTERT, R. T. DWORSKI, B. G. MELLEN, J. A. OATES, J. J. MURRAY, and J. R. SHELLER Prostaglandin E2 Decreases Allergen-stimulated Release of Prostaglandin D2 in Airways of Subjects with Asthma Am. J. Respir. Crit. Care Med., August 1, 2000; 162(2): 637 - 640. [Abstract] [Full Text] [PDF]

				W. Wasiak and M. Szmidt A six week double blind, placebo controlled, crossover study of the effect of misoprostol in the treatment of aspirin sensitive asthma Thorax, October 1, 1999; 54(10): 900 - 904. [Abstract] [Full Text]