Agents that Release Histamine from Mast Cells

Lagunoff, David; Martin, Thomas W.; Read, George

doi:10.1146/annurev.pa.23.040183.001555

Cited by 343 publications

(172 citation statements)

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“…The pan-adenosine receptor (AR) agonist 59-N-ethylcarboxamidoadenosine (NECA), A3R agonist 2-chloro-N 6 -(3-iodobenzyl)-adenosine-59-N-methyluronamide (Cl-IBMECA), A2a receptor antagonist 7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo [1,5-c] pyrimidine (SCH58261), A2b receptor antagonist 8-[4-[((4-Cyanophenyl) carbamoylmethyl) oxy]phenyl]-1,3-di(n-propyl)xanthine hydrate (MRS1754), the A3R antagonist 9-chloro-2-(2-furanyl)-5-((phenylacetyl)amino)- [1,2,4]triazolo [1,5-c] quinazoline (MRS1220), and adenosine deaminase (ADA) were all purchased from Sigma-Aldrich (St. Louis, MO). Ptx was purchased from List Biological Laboratories.…”

Section: Methodsmentioning

confidence: 99%

“…However, their mechanism of action remained largely unresolved. The large repertoire of molecules, including neuropeptides, opiates and the synthetic polyamine compound 48/80 (c48/80), which constitute this family of stimuli (1), their common structural moieties and the fact that micromolar concentrations are required to evoke their biological activity, have suggested that members of this family trigger mast cell activation in a receptor-independent manner (2,3). Consistent with this notion, in vitro studies have demonstrated the ability of members of this family to activate directly Gi proteins (3)(4)(5)(6).…”

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confidence: 99%

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Activation of Mast Cells by Trimeric G Protein Gi3; Coupling to the A3 Adenosine Receptor Directly and upon T Cell Contact

Baram

Dekel

Mekori

et al. 2010

The Journal of Immunology

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Mast cells are key players in mediating and amplifying allergic and inflammatory reactions. Previously, we identified the G-protein, Gi3, as the cellular target of receptor mimetic basic secretagogues that activate mast cell independently of IgE. In this study, we demonstrate that Gi3 is the cellular target of the adenosine A3 receptor (A3R), a G-protein coupled receptor involved in inflammation and the pathophysiology of asthma. By using a cell permeable peptide comprising the C-terminal end of Gαi3 fused to an importation sequence (ALL1) as a selective inhibitor of Gi3 signaling, we show that by coupling to Gi3, the A3R stimulates multiple signaling pathways in human mast cells, leading to upregulation of cytokines, chemokines, and growth factors. We further show that after contact with activated T cell membranes, endogenous adenosine binds to and activates the A3R, resulting in Gi3-mediated signaling. Specifically, the majority of ERK1/2 signaling initiated by contact with activated T cell membranes, is mediated by Gi3, giving rise to ALL1-inhibitable cellular responses. These results unveil the physiological G-protein coupled receptor that couples to Gi3 and establish the important role played by this G-protein in inflammatory conditions that involve adenosine-activated mast cells.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Activation of Mast Cells by Trimeric G Protein Gi3; Coupling to the A3 Adenosine Receptor Directly and upon T Cell Contact

Baram

Dekel

Mekori

et al. 2010

The Journal of Immunology

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“…These cells release histamine in response to both IgE-dependent and non-immunological stimuli (Lagunoff et al, 1983). Non-immunological stimuli include compound 48/80, morphine and the basic peptides substance P. VIP, somatostatin, neurotensin and CGRP (Grosman, 1981;Shanahan et al, 1985;Piotrowski & Foreman, 1986).…”

Section: Introductionmentioning

confidence: 99%

Characterization of neuropeptide‐induced histamine release from human dispersed skin mast cells

Lowman

Benyon

Church

1988

British J Pharmacology

199

103

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1 Human skin mast cells, unlike other human mast cells so far studied, released histamine in a concentration-related manner in response to substance P, vasoactive intestinal peptide (VIP) and somatostatin (1 yM to 30 yM). In contrast, eledoisin, physalaemin, neurokinin A, neurokinin B, calcitonin gene-related peptide (CGRP), neurotensin, bradykinin and Lys-bradykinin induced negligible histamine release. 2 The low histamine releasing activity of physalaemin, eledoisin, neurokinin A and neurokinin B relative to substance P suggests that the human skin mast cell activation site is distinct from the tachykinin NK-1, NK-2 or NK-3 receptors described in smooth muscle.3 The relative potencies of substance P and its fragments SP2 11, SP3 11, SP4_11 and SP1,4 in releasing histamine from human skin mast cells suggests that both the basic N-terminal amino acids and the lipophilic C-terminal portion of substance P are essential for activity. 4 Peptide-induced histamine release, like that induced by compound 48/80, morphine and poly-Llysine, is rapid, reaching completion in 10-20s, is largely independent of extracellular calcium but requires intact glycolysis and oxidative phosphorylation. The substance P analogue, [D-Pro4,D-Trp7'9 "0] SP411 (SPA), not only reduced substance Pinduced histamine release in a concentration-related manner but also inhibited that induced by VIP, somatostatin, compound 48/80, poly-L-lysine and morphine but not anti-IgE. 6 The similar characteristics of histamine release induced by substance P. VIP, somatostatin, compound 48/80, poly-L-lysine and morphine suggest that they share a common pathway of activationsecretion coupling distinct from that of IgE-dependent activation. Furthermore, the ability of human skin mast cells to respond to basic non-immunological stimuli including neuropeptides may reflect a specialised function for these cells.

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“…The morphology of the mast cell degranulation has been studied extensively, and exocytosis is accepted as the degranulation mechanism in rat mast cells. However, most of the in vitro studies (5)(6)(7) were performed by us ing secretagogues, and some differences exist among these degranulation stimuli (8,9). In our previous report, we have described the biochemical and morphological mecha nisms involved in mast cell degranulation in an IgE mediated cell model and the evaluation of the pharma cological properties of anti-allergic agents in type I allergy (10).…”

mentioning

confidence: 99%

Electron Microscopic Studies on the Inhibition of Degranulation of Rat Mast Cells by a Novel Anti-Allergic Agent, PTPC

Ohashi

Watanabe

Nishigaki

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-When rat mast cells sensitized by IgE antibody were exposed to antigen, transmission elec tron microscopy revealed alteration of the granules, cavity formation by fusion of the perigranular mem brane and granule release by the fusion of the cavity membrane with the mast cell membrane. Scanning elec tron microscopy disclosed the extrusion of smooth and round bodies from pores formed on the cell surface. These changes were accompanied by the release of histamine. The inhibition of this degranulation by a novel anti-allergic agent, 6-(1-pyrrolidinyl)-N-(1H-tetrazol-5-yl)-2-pyrazinecarboxamide (PTPC), was evalu ated quantitatively as an inhibition of the granule alteration and cavity formation. At a concentration of 100 nM, PTPC inhibited the granule alteration and cavity formation as well as histamine release. In the same concentration, PTPC significantly increased the cyclic AMP content in the mast cells. These results sug gest that the inhibition of the morphological changes in mast cells by PTPC might be due to the increased cyclic AMP caused by the agent and plays an important role in the suppression of chemical mediators re lease.

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Agents that Release Histamine from Mast Cells

Cited by 343 publications

References 93 publications

Activation of Mast Cells by Trimeric G Protein Gi3; Coupling to the A3 Adenosine Receptor Directly and upon T Cell Contact

Activation of Mast Cells by Trimeric G Protein Gi3; Coupling to the A3 Adenosine Receptor Directly and upon T Cell Contact

Characterization of neuropeptide‐induced histamine release from human dispersed skin mast cells

Electron Microscopic Studies on the Inhibition of Degranulation of Rat Mast Cells by a Novel Anti-Allergic Agent, PTPC

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