Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histamine has remained a putative neurotransmitter for many years, partially because some of the criteria necessary to define it as a central nervous system neurotransmitter have not been established. The demonstration of in vitro release and the quantification of turnover as an indirect measure of release have been complicated by the histological evidence for multiple histamine pools in the central nervous system. In brain, there are multiple cell types which probably contain histamine. These cells include mast cells, neurolipomastocytoid cells, microvascular endothelial cells, and a histaminergic neuronal system which has been visualized using immunocytochemical methods. Using in situ brain microdialysis and a sensitive and specific radioenzymatic assay for histamine, we have identified histamine in the extracellular space of the rat hypothalamus and corpus striatum in vivo. Following neuronal selective stimuli, significant increases in extracellular histamine levels only were observed in the posterior hypothalamus, where dense histaminergic neuronal terminals have been described. However, after manipulations targeted towards histamine-containing mast cells, such increases were seen in both the posterior hypothalamus and corpus striatum. In summary, this study demonstrates that endogenous histamine can be released from the posterior hypothalamus by stimuli targeted towards histamine neurons and that histamine may also be released by non-neuronal mast cell elements.
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PMID:Release of histamine in rat hypothalamus and corpus striatum in vivo. 233 12

The histamine content of uteri from mice was analyzed in terms of both concentration and total amount per uterine horn a) at two stages of the estrous cycle (estrous and diestrous), b) under sex hormone treatment, c) during pregnancy and after delivery. Histamine concentration and mast cell density were greater during diestrous and in mice treated with progesterone (p less than 0.001). This effect was attributed to a reduction in uterine mass weight, since the amount of histamine per uterine horn remained constant throughout the estrous cycle. During pregnancy, both concentration and amount of histamine per uterine horn were increased, values were significantly higher than in estrous (p less than 0.001) from day 14-17 until day 21 when labor occurred. After six to eight hours post-partum an abrupt reduction on histamine content was observed. Mast cells were more abundant in myometrium than in endometrium, their density followed the same pattern as histamine concentration throughout the estrous cycle.
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PMID:Histamine content and mast cells distribution in mouse uterus: the effect of sexual hormones, gestation and labor. 233 18

Five mouse strains, CBA/J, BALB/c, C3H/HeJ, A/J, and C57Bl/6J-bg-bg, all showed similar expulsion kinetics for Nippostrongylus brasiliensis (infective dose = 500 L3). Typically, parasite recovery was maximal on day 2 in the lungs and by day 4 in the small intestine. Few worms (less than 5% infective dose) were recovered on day 14 in all strains. These same mouse strains exhibited immune depression on day 5 of infection with mesenteric lymph node cells (MLN) showing reduced (10-30% normal) IgM, IgG, and IgA responses against heterologous antigen. The intestinal mast cell numbers and tissue histamine levels were examined in CBA/J mice. Mast cell numbers increased (normal = less than 1/villous crypt unit; VCU) from day 5 and peaked on day 12 (greater than 15/VCU). Intestinal histamine levels did not completely correlate with mast cell numbers with maximum concentrations (240 +/- 73 ng/g, 2-fold over normal) reached by day 8. Histamine concentrations in the intestine returned to normal levels by day 20.
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PMID:Characterization of Nippostrongylus brasiliensis infection in different strains of mice. 235 68

Histamine secretion from isolated peritoneal mast cells was inhibited by a number of calmodulin antagonists. The characteristics of the inhibition were consistent with an action after calcium influx. The rank order of potency of the compounds correlated approximately with their reported anti-calmodulin activity. These data provide tentative support for the involvement of calmodulin in stimulus-secretion coupling in the mast cell.
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PMID:Effect of calmodulin inhibitors on histamine secretion from mast cells. 240 48

Histamine inhibits superoxide anion (O-2) production from human neutrophils stimulated by N-formylmethionyl-leucyl-phenylalanine (FMLP). The effects of histamine are dose-dependent and competitively antagonized by cimetidine. When passively sensitized rat serosal mast cells and human neutrophils are mixed together, O-2 production from FMLP-activated granulocytes is significantly reduced, following mast cell degranulation by acetylcholine. These inhibitory effects can be counteracted by cimetidine. Exposure of non-sensitized rat mast cells to FMLP-stimulated human neutrophils causes histamine release. These results suggest bidirectional control mechanisms between mast cells and neutrophils, that further stress the role of histamine in regulating inflammatory processes.
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PMID:Mast cell and neutrophil interactions: a role for superoxide anion and histamine. 240 74

We have studied various functional and morphological characteristics of mast cells obtained in bronchoalveolar lavage from fifty-two patients with several lung diseases. The percentage of mast cells ranged from 0.04 to 0.6% (bronchial carcinoma), 0.05-0.3% (sarcoidosis), 0.06-0.25% (asthma), 0.04-1.8% (miscellaneous) and 0.02-0.04% (normals). There were no significant differences in the mast cell counts between the disease groups. Lung mast cells exhibited heterogeneity of size, shape and intensity of staining. Cells from thirty-seven subjects were further studied for total histamine content and histamine release using various secretagogues. There was a significant correlation (P less than 0.001) between the histamine content of the total lavage cell population and mast cell counts. The calculated mean histamine content per mast cell was 6.35 pg. Histamine was released in a dose-dependent fashion after stimulation with anti-IgE, calcium ionophore and phorbol myristate acetate with a time course of histamine release characteristic of the mast cell. Unlike peripheral blood basophils, no release was observed following incubation with f-met-leu-phe (10(-6)-10(-8) M) and neither cell type released histamine following incubation with 48/80 (10 micrograms/ml). Inhibition of anti-IgE-induced histamine release was obtained following pre-incubation with salbutamol (10(-4)-10(-6) M). These studies indicate that bronchoalveolar lavage is a suitable model for the study of human lung mast cells.
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PMID:Morphological and secretory properties of bronchoalveolar lavage mast cells in respiratory diseases. 242 72

Early transient incapacitation (ETI) is the complete cessation of performance during the first 30 min after radiation exposure and performance decrement (PD) is a reduction in performance at the same time. Supralethal doses of radiation have been shown to produce a marked decrease in regional cerebral blood flow in primates concurrent with hypotension and a dramatic release of mast cell histamine. In an attempt to elucidate mechanisms underlying the radiation-induced ETI/PD phenomenon and the postradiation decrease in cerebral blood flow, primates were exposed to 100 Gy (1 Gy = 100 rads), whole-body, gamma radiation. Pontine and cortical blood flows were measured by hydrogen clearance, before and after radiation exposure. Systemic blood pressures were determined simultaneously. Systemic arterial histamine levels were determined preradiation and postradiation. Data obtained indicated that radiated animals showed a decrease in blood flow of 63% in the motor cortex and 51% in the pons by 10 min postradiation. Regional cerebral blood flow of radiated animals showed a slight recovery 20 min postradiation, followed by a fall to the 10 min nadir by 60 min postradiation. Immediately, postradiation systemic blood pressure fell 67% and remained at that level for the remainder of the experiment. Histamine levels in the radiated animals increased a hundredfold 2 min postradiation. This study indicates that regional cerebral blood flow decreases postradiation with the development of hypotension and may be associated temporally with the postradiation release of histamine.
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PMID:Postradiation regional cerebral blood flow in primates. 242 23

To investigate the possible role of mast cells in blood vessel formation, rat mast cell granules were studied for their proliferative effect on human microvascular endothelial cells. It was found that granules had a marked proliferative effect and that most of this activity was restricted to a dialyzable fraction. The dialyzable mast cell granule constituent histamine was found to be mitogenic, an effect that was shown with the use of specific agonists and antagonists to be mediated through an H1 receptor. H1 antagonists reduced the proliferation caused by the untreated mast cell granules to the level of proliferation caused by dialyzed granules, suggesting that all the dialyzable mitogenic activity was due to histamine. Histamine was also shown to cause proliferation of cells that were growth arrested by serum deprivation, suggesting that it is an endothelial growth factor. The compound responsible for the undialyzable mitogenic activity could not be identified but was shown not to be mast cell heparin. This demonstration of mast cell granule-induced endothelial proliferation suggests that the mast cell may be of importance in the process of angiogenesis.
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PMID:Mast cell granules cause proliferation of human microvascular endothelial cells. 242 96

Intravenous administration of morphine sulfate often produces urticarial and hypotensive reactions associated with elevations in plasma histamine. The source of this histamine and mechanisms controlling its release are poorly understood. Previous studies of morphine-induced histamine release compared human leukocytes to rat peritoneal mast cells. The effects of morphine on human cutaneous mast cells has not been examined. We studied in vitro histamine release from human basophils and human skin preparations containing cutaneous mast cells to evaluate their relative contribution to the pharmacologic effects of morphine. Human skin mast cell preparations showed dose-dependent histamine release over a morphine concentration range of 1.5 X 10(-5) to 4.5 X 10(-3) M, with peak release occurring at 5 X 10(-4) M, with peak release occurring at 5 X 10(-4) M. Clinically, morphine sulfate is usually injected as a 1.5 X 10(-2) M solution. Histamine release was calcium dependent and equivalent to that obtained with 3 and 10 mM strontium. Morphologic examination revealed degranulation and exocytosis occurring in morphine-stimulated tissue but not in specimens exposed to buffer alone. Lactate dehydrogenase levels did not increase following morphine incubation, thus supporting a noncytolytic mechanism of histamine release. Basophils, in contrast, showed no significant histamine release from exposure to morphine up to 10(-2) M. Concanavalin A, as a positive control in these same preparations, produced a mean histamine release of 21.0%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Functional differences between human cutaneous mast cells and basophils: a comparison of morphine-induced histamine release. 242 25

Histamine released from skin mast cells in normal skin sites of patients with idiopathic chronic urticaria (CU) and normal volunteers was assessed with the skin chamber technique. Small amounts of histamine were spontaneously and continuously released during the 4-hour observation in both groups but were twofold greater in patients with CU. In addition, histamine levels were significantly more elevated in sites challenged with compound 48/80 than in unstimulated sites. Patients with CU differed from normal volunteers in that histamine release induced by 48/80 compound was significantly greater at 1 and 2 hours after challenge. The number of mast cells and the histamine content of the skin did not differ in the two groups. These observations could suggest a functional defect at the mast cell level rather than a difference in their numbers.
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PMID:Increased compound 48/80 induced local histamine release from nonlesional skin of patients with chronic urticaria. 243 Oct 27


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