scholarly journals Regulation of plasma histamine levels by the mast cell clock and its modulation by stress

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Yuki Nakamura ◽  
Kayoko Ishimaru ◽  
Shigenobu Shibata ◽  
Atsuhito Nakao
Keyword(s):  
1997 ◽  
Vol 6 (1) ◽  
pp. 25-31 ◽  
Author(s):  
J. Carvalho Tavares ◽  
A. Moreno ◽  
M. Sánchez Crespo

The purpose of this study is to assess the role of nitric oxide (NO) in the intestinal lesions of passive anaphylaxis, since this experimental model resembles necrotizing enterocolitis. Sprague-Dawley rats were sensitized with IgE anti-dinitrophenol monoclonal antibody. Extravasation of protein-rich plasma and haemorrhagia were measured in the small intestine. Plasma histamine was measured to assess mast cell activation. The effect of exogenous NO on the lesions was assessed by using two structurally unrelated NO-donors: sodium nitroprusside and S-nitroso-Nacetyl-penicillamine (SNAP). An increased basal production of NO was observed in cells taken after anaphylaxis, associated with a reduced response to platelet-activating factor, interleukin 1beta, and IgE/DNP-bovine serum albumin complexes. The response to bacterial lipopolysaccharide and dibutyryl cyclic adenosine monophosphate (AMP) was enhanced 24 h after challenge, but at earlier times was not significantly different from that observed in controls. Treatment with either sodium nitroprusside or SNAP produced a significant reduction of the haemorrhagic lesions, which are a hallmark of rat anaphylaxis. The extravasation of protein-rich plasma was not influenced by NO-donors. The increase of plasma histamine elicited by the anaphylactic challenge was not influenced by SNAP treatment. NO-donors protect intestinal haemorrhagic lesions of rat anaphylaxis by a mechanism apparently independent of mast cell histamine release.


1989 ◽  
Vol 87 (6) ◽  
pp. 649-654 ◽  
Author(s):  
Beth S. Friedman ◽  
Susan C. Steinberg ◽  
William J. Meggs ◽  
Michael A. Kaliner ◽  
Marianne Frieri ◽  
...  
Keyword(s):  

Author(s):  
Taylor L. Curley ◽  
Douglas H. Thamm ◽  
Sam W. Johnson ◽  
Pedro Boscan

Abstract OBJECTIVE To determine the effects of morphine on histamine release from 2 canine mast cell tumor (MCT) cell lines and on plasma histamine concentrations in dogs with cutaneous MCTs. ANIMALS 10 dogs with cutaneous MCT and 10 dogs with soft tissue sarcoma (STS). PROCEDURES The study consisted of 2 phases. First, 2 canine MCT cell lines were exposed to 3 pharmacologically relevant morphine concentrations, and histamine concentrations were determined by an ELISA. Second, dogs with MCT or STS received 0.5 mg of morphine/kg, IM, before surgery for tumor excision. Clinical signs, respiratory rate, heart rate, arterial blood pressure, rectal temperature, and plasma histamine concentrations were recorded before and 5, 15, 30, and 60 minutes after morphine administration but prior to surgery. Data were compared by use of a 2-way ANOVA with the Sidak multiple comparisons test. RESULTS In the first phase, canine MCT cell lines did not release histamine when exposed to pharmacologically relevant morphine concentrations. In the second phase, no differences were noted for heart rate, arterial blood pressure, and rectal temperature between MCT and STS groups. Plasma histamine concentrations did not significantly differ over time within groups and between groups. CONCLUSIONS AND CLINICAL RELEVANCE No significant changes in histamine concentrations were noted for both in vitro and in vivo study phases, and no hemodynamic changes were noted for the in vivo study phase. These preliminary results suggested that morphine may be used safely in some dogs with MCT.


2005 ◽  
Vol 230 (9) ◽  
pp. 681-687 ◽  
Author(s):  
Sang-Hyun Kim ◽  
Tae-Yong Shin

In this study, we investigated the effect of Amomum xanthiodes (Zingiberaceae) extract (AXE) on the mast cell-mediated allergy model and studied the possible mechanism of action. We found that AXE inhibited compound 48/80-induced systemic reactions and plasma histamine release in mice. Additionally, AXE decreased immunoglobulin E (IgE)-mediated local allergic reactions and passive cutaneous anaphylaxis (PCA), and AXE dose-dependently attenuated the release of histamine from rat peritoneal mast cells (RPMC) activated by compound 48/80 or IgE. The amounts of AXE needed for inhibition of compound 48/80-induced plasma histamine release and PCA were similar to disodium cromoglycate, the known anti-allergic drug. We found that AXE increased the cAMP levels and decreased the compound 48/80-induced intracellular Ca2+. Furthermore, AXE attenuated the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore (A23187)-stimulated tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 secretion in human mast cells. The inhibitory effect of AXE on the proinflammatory cytokines was nuclear factor-κB (NF-κB)-dependent. In addition, AXE decreased PMA plus A23187-induced degradation of IκBα and the nuclear translocation of NF-κB. Our findings provide evidence that AXE inhibits mast cell-derived immediate-type allergic reactions, and that cAMP, intracellular Ca2+, proinflammatory cytokines, and NF-κB are involved in these effects.


1981 ◽  
Vol 61 (2) ◽  
pp. 159-162 ◽  
Author(s):  
P. J. Barnes ◽  
M. J. Brown

1. Venous plasma histamine was measured by a specific and sensitive radioenzymatic assay in seven male extrinsic asthmatic and six age-matched non-atopic non-asthmatic male subjects during exercise and voluntary isocapnic hyperventilation. 2. There was no change in peak expiratory flow in normal subjects with exercise or hyperventilation, but asthmatic subjects showed a 29.4 ± sem 5.8% fall after exercise and a 29.0 ± 5.4% fall after matched hyperventilation. 3. Plasma histamine was significantly higher (P < 0.05) in asthmatic (6.2 ± 0.95 nmol/l) than that in normal subjects (3.4 ± 0.61 mmol/l) and showed a significant (P < 0.01) rise (to 14.4 ± 1.83 nmol/l) during exercise in asthmatic, but not in normal subjects. This suggests that discharge of mast-cell mediators may occur during exercise in asthmatic subjects who develop exercise-induced asthma. 4. With hyperventilation there was no change in plasma histamine in either asthmatic or normal subjects, but this does not exclude the possibility that mediators may be released locally in the airways.


1977 ◽  
Vol 43 (2) ◽  
pp. 271-275 ◽  
Author(s):  
W. M. Gold ◽  
G. L. Meyers ◽  
D. S. Dain ◽  
R. L. Miller ◽  
H. R. Bourne

We studied the effect of inhaled specific antigen on airflow resistance, histamine concentration, and mast cell numbers in airway tissues in allergic dogs. In each of six allergic dogs with open chests, inhalation of specific antigen aerosol (Ascaris suum) increased airflow resistance from 0.30+/-0.40 (mean+/-SE) to 2.8+/-0.41 cmH2O/1 per s (P less than 0.05); decreased mast cell number from 38.6+/-3.2 to 24.3+/-4.5 mast cells/mm2 (P less than 0.05); decreased histamine (per mg airway tissue) from 5.3+/-0.4 to 3.5+/-0.2 ng (P less than 0.05) in lobar bronchi 5–7 mm in diam; and released histamine into the blood perfusing the lung, control arterial plasma histamine; 2.8+/-0.64 ng/ml; antigen: 154+/-1.7 ng/ml (P less than 0.005). Specific antigen caused no significant changes in mast cells or histamine in bronchi 1–2 mm in diam. Control aerosols of nonspecific antigen or methacholine did not change levels of mast cells or histamine in airway tissues. These results suggest that experimental canine asthma involves local airway reactions with degranulation of mast cells and histamine release, as well as vagally mediated reflex bronchoconstriction.


2010 ◽  
Vol 20 (3) ◽  
pp. 209-215
Author(s):  
Allison van Gelderen ◽  
Joy Archer ◽  
Michael E. Herrtage
Keyword(s):  

1990 ◽  
Vol 4 (5) ◽  
pp. 242-246 ◽  
Author(s):  
Leslie E. Fox ◽  
Robert C. Rosenthal ◽  
David C. Twedt ◽  
Richard R. Dubielzig ◽  
E. Gregory MacEwen ◽  
...  

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