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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The i.p. administration of L-histidine in doses of 500 and 1000 mg/kg, caused prolonged high levels of histidine but did not influence the levels of histamine in the non-mast cell tissues such as the stomach, lungs and liver in the rat. After polymyxin B or 48/80 treatments as well as in anaphylaxis, the levels of histamine in the lungs and liver were greatly reduced but histidine administration failed to alter noticeably the concentrations of histamine in these organs. Similarly, the low contents of histamine in the stomach of 48/50-treated or polymyxin B-treated rats remained unchanged in the presence of excess histidine. Histidine loadings however produced a marked increase in histidine decarboxylase activity of the glandular stomach and a simultaneous elevation in the serum histamine concentrations. Results suggest that the increased level of serum histamine is the consequence of the increased activity of histidine decarboxylase in the tissues and a rapid elimination of the newly formed histamine into the blood. This led us to consider that the flux rather than the formation of histamine might be regulatory for the actual concentration of the non-mast cell histamine, especially in stomach tissue.
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PMID:Non-mast cell histamine levels in rat tissues after histidine loading. 85 8

Subcellular fractionation techniques, radio-labeling by the 3H-precursor and pharmacological approach applied to the developing rat indicate the presence of at least two types of histamine-containing cells in brain. The presence of the histamine synthesizing enzyme in neurons is suggested by its developmental pattern: there is a 4- to 5-fold increase in enzyme activity from birth to adulthood, with a time-course paralleling the synaptogenesis in whole brain as well as in the 4 regions studied (medulla-pons, midbrain, hypothalamus and forebrain). As is the case for different transmitter synthesizing enzymes such as tyrosine hydroxylase, there is a shift in the subcellular distribution of histidine decarboxylase (H.D.) activity from the soluble fraction at birth to the synaptosomal fraction in the adult brain. On the other hand, several lines of evidence indicates that a portion of histamine is localized, at least in the noenatal rat brain, in mast cells: (a) the high level of histamine in the neonatal rat brain is, like in peripheral mast-cells, associated with a low enzyme activity; (b) the half-life of [3H]histidine injected s.c. at birth was about 4 days, a value close to that found in skin (a tissue rich in mast cells), but contrasting with that in adult brain (less than 1 h); (c) after subcellular fractionation, the endogenously formed [3H]histamine was recovered in the crude nuclear fraction as was the amine from peritoneal mast cells added to the brain homogenate; (d) the mast cell degranulators, compound 48/80 and polymyxin B, induce a small but significant release of the amine from incubated neonatal brain slices. Thus it appears that cerebral histamine is localized in at least two cell types. Its presence in neurons is compatible with a neurotransmitter function and its release from mast cells might represent some primitive form of cell-to-cell communication.
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PMID:Histamine synthesis in the developing rat brain: evidence for a multiple compartmentation. 110 98

In the rat, gastric histamine is stored predominantly in the enterochromaffin-like (ECL) cells, which are located basally in the oxyntic mucosa. The functional significance of histamine in the ECL cells is a matter of speculation. In this study the effect of depletion of histamine on the properties and ultrastructure of the ECL cells was examined. Histamine synthesis was inhibited with alpha-fluoromethylhistidine (3 mg.kg-1.h-1) given via osmotic minipumps over a period of 24 h. The treatment reduced the histidine decarboxylase activity (approximately 20% remaining) and histamine concentration (less than 20% remaining) in the oxyntic mucosa, as well as the intensity of histamine- and chromogranin A-immunostaining in the ECL cells, compared to control rats. The cytoplasmic (secretory) granules/vesicles were greatly reduced in number and size following alpha-fluoromethylhistidine administration. The histamine immunostaining of the mast cells, which occurs at the mucosal surface and in the submucosa, appeared unaffected. We conclude that ECL cell histamine accounts for at least 80% of the total oxyntic mucosal histamine in the rat and that it represents a more mobile pool than mast cell histamine. The reduction in the number and size of the ECL cell granules/vesicles following histamine depletion is in accord with the idea that they represent the storage site for histamine.
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PMID:Enterochromaffin-like cells in the rat stomach: effect of alpha-fluoromethylhistidine-evoked histamine depletion. A chemical, histochemical and electron-microscopic study. 138 83

Fasting gastrinemia, fundic argyrophil cell density, mast cell number, basal fundic histamine content and histidine decarboxylase activity were determined in 20 antrectomized patients and 20 control subjects. Fasting gastrinemia and fundic argyrophil cell density were significantly lower in antrectomized patients than in controls, whereas fundic mast cell number, basal histamine content, and histidine decarboxylase activity did not differ significantly between the two groups. In antrectomized patients the basal fundic histamine content appears related to the fundic mast cell number, as a consequence of the reduced effect of gastrin on argyrophil cells.
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PMID:Argyrophil cells, mast cells, and histamine in the fundic mucosa of antrectomized patients. 143 47

The effect of intracerebroventricularly (i.c.v.) administered histamine (100 micrograms/rat) on intestinal myoelectrical activity was investigated in the jejunum of fasted rats. Histamine caused the disappearance of phase III and a partial reduction of phase II of migrating myoelectric complexes. This effect was antagonized by i.c.v. pretreatment with mepyramine (10 micrograms/rat), an H1 receptor antagonist. Lesions of central noradrenergic neurons by i.c.v. injection of the neurotoxin 6-hydroxydopamine strongly reduced both the inhibition of intestinal propulsion and the migrating myoelectric complexes profile induced by i.c.v. histamine, whereas pretreatment with p-chlorophenylalanine, a selective depletor of serotonin stores, had no effect. It thus appears that aminergic pathways are involved in the visceral effects of central histamine. Mepyramine (200 micrograms/rat i.c.v.) partially reduced the slowing of intestinal transit induced by high doses of morphine. Pretreatment with compound 48/80 (10 micrograms/rat i.c.v.), a mast cell degranulator, but not with alpha-fluoromethylhistidine, an irreversible inhibitor of histidine decarboxylase, reduced the antipropulsive action of i.c.v. morphine to the same extent as mepyramine, suggesting that histamine released from cerebral mast cells by high doses of morphine could contribute to the intestinal inhibition by morphine.
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PMID:Further investigations on the antipropulsive effect of centrally administered histamine and its relation with morphine. 161 2

Several parameters connected to histamine metabolism and mast cell number were examined in the lungs of rats infected with the nematode Nippostrongylus brasiliensis. Histamine levels as well as mast cell numbers were found to be increased on day 14 after infection and were elevated during the whole time of the experiment. Histidine decarboxylase activity also reached a peak on day 14. There was no measurable activity of diamine oxidase in the lungs of parasitized and normal rats. It is postulated that the increase in histidine decarboxylase activity and histamine concentration observed in the present study is related to the process of mastocytosis.
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PMID:Histamine metabolism in lungs of rats infected with Nippostrongylus brasiliensis. 211 40

Previous work from this laboratory had indicated that in vivo, histidine decarboxylase (HDC) activity was stimulated by compound 48/80 in rat leg muscle, and that high dietary calcium had a stimulating effect on gastric HDC activity. In the present investigations the 48/80 effect was also observed in vitro in leg muscle extracts from rats, chicks, and guinea pigs. Compound 48/80 had no effect in vitro on histamine metabolism of gastric tissue homogenates in any of the animal species studied. A dietary effect of high calcium intake was noted in rat gastric tissue but not in rat leg muscle. In vitro addition of 48/80 and/or calcium had no stimulatory effect on bacterial HDC or on muscle carnosinase activity. These findings, in conjunction with a comparison of stomach and leg muscle mast cell populations, confirm an HDC stimulatory role for 48/80 in muscle, in addition to its histamine-releasing function from mast cells.
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PMID:Differential response of muscle and gastric histidine decarboxylase to compound 48/80 and dietary calcium. 241 63

When peritoneal resident cells (PRCs) of genetically mast cell-deficient WBB6F1-W/Wv mice were cultured in vitro for 5 h at 37 degrees C, their histidine decarboxylase [HDC, L-histidine carboxylase, E.C. 4.1.1.22] activity increased 10-fold. Since inhibitors for energy production and mRNA and protein syntheses inhibited this increase of HDC activity, it appeared to represent de novo synthesis of the enzyme, i.e., induction. This increase was followed by an increase in the amount of histamine in the culture medium of the cells, indicating that histamine synthesized by the induced HDC was not stored in the cells but was quickly released. Mast cells were not involved in the HDC induction, because the extents of HDC induction in PRCs of W/Wv and wild type +/+ mice were similar. The removal of T cells with anti-Thy-1,2 antibody and complement from the PRCs did not affect the HDC induction, but the removal of phagocytes decreased the induction to one-tenth in spite of a 2-fold increase in the proportion of B cells in the PRCs. After separation of the PRCs into adherent and non-adherent fractions, the increase in HDC activity was found to be associated with the adherent fraction that was mostly positive to esterase staining. These results suggest that HDC was induced in peritoneal macrophages.
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PMID:In vitro increase of histidine decarboxylase activity and release of histamine by peritoneal resident cells of mast cell-deficient W/Wv mice; possible involvement of macrophages. 245 55

N-Acetyl-aspartyl magnesium glutamate (Rhinaaxia, NAAGA) is a topically active antiallergic dipeptide. The compound acts in two different ways. On the one hand NAAGA inhibits the mast cell-degranulation, on the other hand this compound blocks the activation of the C3-convertase, subsequently followed by a blocked cleavage of the fragments C3a and C5a, respectively. 20 patients suffering from pollinosis were treated for 2 weeks according to a randomized double-blind placebo-controlled study. Besides subjective complaints nasal obstruction was objectively documented via rhinomanometria. 9 out of 10 patients under placebo had to use the rescue drug tritoqualine, a histidine decarboxylase inhibitor, compared to none in the verum group (p less than 0.01). After 14 days of treatment with NAAGA the nasal peak flow rate increased by 21.5 l/min and 21.8 l/min in the tritoqualine/placebo group, respectively (not significant). Nasal obstruction improved statistically significantly after 7 and 14 days of treatment in both groups. Tolerance was reported to be good in either group.
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PMID:[Effectiveness and tolerance of the C3 convertase inhibitor, N-acetyl-aspartyl-magnesium glutamate with anti-allergic action. Results of a double-blind study]. 265 2

Like the skin of rats and mice injected with adrenaline (AD), rat isolated peritoneal mast cells display increased levels of perchloric acid-soluble histamine following incubation with AD. Although pre-exposure to alpha-fluoromethyl histidine (FMH), an inhibitor of histidine decarboxylase, prevented the effect of AD in vivo and in vitro, this compound was also found to inhibit mast cell granule swelling evoked by AD, a response linked to histamine changes. Absence of increased levels of isotopic histamine in mast cells incubated with labelled histidine in the presence of AD, as well as the insufficient amounts of would-be precursor histidine found in untreated mast cells, confirm the conclusion that AD does not increase mast cell histamine by stimulating its synthesis.
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PMID:Increased levels of histamine observed in the skin of adrenaline-treated rats or mice are not the result of histamine synthesis by mast cells. 275 May 95


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