Is prostaglandin a mediator for the inhibitory action of histamine, hydrocortisone, and isoproterenol?

C. Staszak, James Goodwin

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

We examined the inhibitory actions of prostaglandin E2, histamine, isoproterenol, hydrocortisone, and interferon on lymphocyte mitogenesis. There was a high degree of intercorrelation between the amount of inhibition caused by prostaglandin E2, histamine, isoproterenol, and hydrocortisone, but not interferon, in any given subjects; that is if lymphocytes from a given subject were highly sensitive to inhibition by one of those agents, they were also sensitive to the other agents. The inhibitory actions of histamine, isoproterenol, or hydrocortisone could be partially blocked by adding prostaglandin synthetase inhibitors to the mitogen cultures. Preincubation of the lymphocytes for 18 hr prior to the addition of mitogens and inhibitors resulted in a loss in sensitivity to the inhibitors other than interferon. Removal of glass-adherent cells (the prostaglandin-producing cells) prior to culture lessened the inhibition caused by histamine and isoproterenol. The above data would suggest that these inhibitors may act via prostaglandin; however, all of these compounds actually decrease prostaglandin production in cultures of peripheral blood mononuclear cells. The implications of these findings are discussed.

Original languageEnglish (US)
Pages (from-to)351-361
Number of pages11
JournalCellular Immunology
Volume54
Issue number2
StatePublished - 1980
Externally publishedYes

Fingerprint

Isoproterenol
Histamine
Prostaglandins
Hydrocortisone
Interferons
Lymphocytes
Mitogens
Dinoprostone
Prostaglandin Antagonists
Prostaglandin-Endoperoxide Synthases
Glass
Blood Cells

ASJC Scopus subject areas

  • Cell Biology
  • Immunology

Cite this

Is prostaglandin a mediator for the inhibitory action of histamine, hydrocortisone, and isoproterenol? / Staszak, C.; Goodwin, James.

In: Cellular Immunology, Vol. 54, No. 2, 1980, p. 351-361.

Research output: Contribution to journalArticle

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