Journal ArticleDOI
Inhibition of Histamine Release by Histamine controlled by H2 Receptor
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It is suggested that histamine could “feedback” to control the spread of an allergic response by decreasing the response of other target cells (tissue mast cells, blood basophils) to an allergenic challenge.Abstract:
AGENTS which increase the intracellular level of adenosine 3′-5′-monophosphate (cyclic AMP) in human leukocyte preparations such as the catecholamines, methylxanthines and prostaglandins, inhibit the antigen induced, IgE antibody mediated release of histamine from human leukocytes (basophils)1–3 Not only are the dose response relationships for increased cyclic AMP levels and the inhibition of histamine release similar, but the kinetics of the two events are also parallel and it is accepted as a working hypothesis that changes in the cyclic AMP level of human basophils (and mast cells) modulate the in vitro allergic response4–6 Recently, we showed that exogenous histamine could increase the cyclic AMP level of human leukocyte preparations and stop the release of endogenous histamine This occurred at concentrations of histamine (about 10−6 M) which are present in the cell suspension under study7 For this reason we suggested that histamine could “feedback” to control the spread of an allergic response by decreasing the response of other target cells (tissue mast cells, blood basophils) to an allergenic challenge No clear effect of antihistamines on the inhibition of histamine release by histamine was observed: concentrations up to 10−3 M to 10−4 M of several antihistamines had little effect and higher concentrations of these drugs either caused inhibition of histamine release themselves or were cytotoxic2,7read more
Citations
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Journal ArticleDOI
Modulation of Inflammation and Immunity by Cyclic AMP
Henry R. Bourne,Lawrence M. Lichtenstein,Kenneth L. Melmon,C S Henney,Yacob Weinstein,Gene M. Shearer +5 more
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Mast cells and basophils.
TL;DR: It is shown that mast cells and allergic mechanisms play at least some role in bronchial asthma and the incidence of these mechanisms in a cross section of all asthmatics is high.
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Pseudomonas stutzeri YPL-1 Genetic Transformation and Antifungal Mechanism against Fusarium solani, an Agent of Plant Root Rot
TL;DR: In several biochemical tests with culture filtrates of P. stutzeri YPL-1 and in mutational analyses of antifungal activities of reinforced or defective mutants, it is found that the anti-F.
References
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Journal ArticleDOI
Definition and antagonism of histamine H 2 -receptors.
TL;DR: H2-receptor antagonist, a new group of drugs, may help to unravel the physiology of histamine and gastrin.
Journal ArticleDOI
A simple and sensitive saturation assay method for the measurement of adenosine 3':5'-cyclic monophosphate.
Journal ArticleDOI
Studies on the mechanisms of hypersensitivity phenomena. ix. histamine release from human leukocytes by ragweed pollen antigen.
TL;DR: It has been proposed that immunologically induced histamine release is an active, enzymatically mediated process which occurs as a multistep response of viable cells to a specific antigenic stimulus.
Journal ArticleDOI
Histamine release in vitro: inhibition by catecholamines and methylxanthines.
TL;DR: Methylxanthines and catecholamines both inhibit antigenically induced histamine release from human leukocytes, but must be present when antigen is added; preincubation is not effective.
Journal ArticleDOI
Immunological release of histamine and slow-reacting substance of anaphylaxis from human lung : I. Modulation by agents influencing cellular levels of cyclic 3',5'-adenosine monophosphate.
TL;DR: In this article, drugs capable of increasing cellular levels of CAMP such as beta-adrenergic agents and methylxanthines inhibit the antigen-induced release of both histamine and SRS-A from human lung and these agents demonstrate synergism when used together.
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