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)

Blood flow was determined in weal and flare reactions and in late dermal reactions after skin-prick tests with allergen, histamine, bradykinin and compound 48/80 in pollen-allergic subjects. Local blood flow was measured with laser Doppler flowmetry intermittently for up to 48 hr at three distances from the prick centre (2 mm; weal, 15 mm; flare and 30 mm). Continuous recordings were also made in the weal area after challenge with bradykinn and compound 48/80. The size of the induced weal and flare area of all the substances and the late phase after allergen was determined using digitized planimetry. Furthermore, simultaneous determinations of local dermal temperature and blood flow in the weal and flare site were performed intermittently for 6 hr after allergen and histamine challenges. There was a dose-dependent and distance-related increase in blood flow for all the substances tested. The blood flow in the 2-mm registrations had normalized 20 min after bradykinin, 1.5-2 hr after histamine and 3 hr after compound 48/80, while allergen induced a continuous increase in blood flow for more than 24 hr. The area of the weal and flare reaction was dose related for all substances, and a similar dose-dependent increase was noted for the observed dermal late-phase reactions present after allergen. The local temperature after challenge with allergen and histamine was also increased in a distance-dependent manner. These studies suggest that laser Doppler flowmetry is a sensitive and reproducible method to quantify blood flow changes occurring after skin-prick tests. Different putative mediators or mast cell stimulating substances produce various response profiles, all of which differ from those observed after allergen. Temperature measurements after skin-prick tests seem to follow the observed changes in blood flow as measured with laser Doppler flowmetry, which may be why both techniques might reflect changes in capillary blood flow.
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PMID:Dermal blood flow after local challenges with allergen, histamine, bradykinin and compound 48/80. 186 96

The present study was conducted to investigate whether a single administration of a relatively low dose of 8-methoxypsoralen (8-MP) with long-wave ultraviolet A (UVA) irradiation alters human skin test responses to a mast cell secretagogue, codeine, and to a vasodilator, histamine. Administration of 8-MP at a dose of 10 mg followed by UVA irradiation (1 joule/cm2) suppressed the skin flare-and-wheal response to codeine and decreased the number of visible degranulated mast cells in biopsy specimens examined histologically. UVA irradiation alone enhanced the skin wheal-and-flare response to either codeine or histamine. The inhibitory effect of 8-MP plus UVA irradiation on both wheal-and-flare responses to codeine tended to decrease, and an increasing enhancement of the skin response to histamine could be observed as the dose of 8-MP was increased from 10 to 30 mg. We postulate that (1) a single 8-MP plus UVA irradiation treatment at appropriate doses could be a potential approach to modulate the mediator-releasing properties of mast cells resident in the skin and (2) the underlying mechanisms of this inhibition is complex, probably reflecting a balance between the inhibitory effect of 8-MP plus UVA irradiation on mast cell-mediator release, enhancement of the vascular response to histamine, and direct photoactivation of resident mast cells.
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PMID:Modulation of human cutaneous mast cell responsiveness by a single, low-dose, PUVA treatment. 189 Feb 69

Pruritus is a common symptom associated with chronic renal failure (CRF). But increased plasma histamine levels and skin mast cell proliferation previously reported in these patients did not correlate with the intensity of the pruritus. Since increased mast cell releasability was described in chronic idiopathic urticaria, we attempted to examine whether this mechanism could explain pruritus in patients with CRF. Twenty-five patients with end stage renal failure were skin tested with histamine, codeine, and compound 48/80. There were nine patients on continuous ambulatory peritoneal dialysis, eight patients on hemodialysis, (tested both before and after dialysis) and eight patients with advanced CRF. Wheal area after intradermal injection of three concentrations of the above substances was measured. In general, the wheal areas in all patients with CRF were either similar to or smaller than those of the control group who were without renal impairment. In conclusion, patients with CRF with or without dialysis therapy demonstrated unchanged or decreased skin test responses to histamine, codeine, and compound 48/80. Increased mast cell releasability cannot explain the pruritus in patients with CRF.
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PMID:Cutaneous responses to histamine, compound 48/80, and codeine in patients with chronic renal failure. 195 8

The intention of the present study was to compare formoterol and terbutaline regarding ability to inhibit immediate wheal and flare responses (WFR) to anti-human IgE with focus on the duration of anti-WFR action. Formoterol is a novel beta 2-adrenergic agonist with a prolonged duration of bronchodilation capacity after inhalation. The drugs injected intradermally 2 min prior to challenge with anti-IgE in volunteers produced a dose-dependent inhibition of the WFR in the range 1pg-100ng (formoterol) and 1ng-1 microgram (terbutaline). Formoterol was 70 times (flare) and 25 times (wheal) more potent (ID40) than terbutaline on a weight basis. The duration of the anti-WFR action for formoterol, injected in a 25 times lower dose than terbutaline, was significantly longer, namely greater than 24 h versus 8 h for terbutaline. The histamine-induced wheal reaction was attenuated by 15% and 25% by terbutaline and formoterol, respectively. The results indicate a higher beta 2-receptor activity for formoterol with respect to inhibition of IgE-dependent mast cell mediator release in addition to an anti-leak effect exerted by both drugs. The prolonged duration of antagonistic effect by formoterol on the WFR to anti-IgE might be due to the lipophilic property of the drug, with an expected higher retention of formoterol at the target tissue compared with the more hydrophilic compound terbutaline.
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PMID:Inhibition of anti-IgE induced skin response in normals by formoterol, a new beta 2-adrenoceptor agonist, and terbutaline. 1. Dose response relation and duration of effect on the early wheal and flare response. 197 24

Neutrophil attractant/activation protein-1 (NAP-1) is a recently described cytokine that attracts neutrophils, but not monocytes or eosinophils. This leukocyte specificity is not absolute, in that NAP-1 attracts basophils and small numbers of lymphocytes. Our purpose was to determine in vivo effects of NAP-1, and to compare them to the reported action of the complement attractant, C5a. Intradermal injection into normal human subjects of 40 microliters of NAP-1, over a concentration range of 4 x 10(-8) M to 10(-6) M, caused no symptoms or signs such as wheal-and-flare, itching, induration, or tenderness. However, biopsies of injection sites showed perivascular neutrophil infiltration as early as 30 min, which increased at 1 and 3 h. The mean number of neutrophils per mm2 of dermis for 15 biopsies taken 3 h after intradermal injection of 2 x 10(-7) M or 10(-6) M NAP-1 was 164 +/- 41; the response to saline or a NAP-1 inactive fragment was 5 or less. Intradermal NAP-1 did not cause basophil or lymphocyte infiltration. Consistent with the absence of a wheal-and-flare, acid toluidine blue-stained sections showed no evidence of mast cell degranulation, in contrast to previously reported results with C5a. Thus, the predominant response by human subjects to intradermal NAP-1 was neutrophil accumulation in proximity to dermal blood vessels.
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PMID:Neutrophil recruitment by intradermally injected neutrophil attractant/activation protein-1. 202 77

A 24 year old man developed severe asthma two years after starting to work in a plywood plant. Four years later the patient had to stop working because of the increasing severity of his asthma. Three months after leaving his job, the patient's asthma was greatly improved. His job consisted of placing plywood sheets into a drying machine. The plywood sheets had stayed outside in wet conditions for at least four to six weeks and were usually covered with moulds. Drying the plywood sheets changed the mould into a fine orange powder. Exposure to this in the laboratory induced an isolated immediate asthmatic reaction. The same reaction was seen when the patient was challenged with an extract of the mould powder at a 0.1% w/v concentration. Skin prick test with the mould extract induced a weal and flare reaction and IgE antibodies against the dry mould powder were identified. A control patient with the same degree of bronchial hyperreactivity did not have any asthmatic reaction when challenged with the same mould extract. Culture of the dry mould powder on Sabouraud agar plates grew pure Neurospora sp. This mould has not been previously reported as a cause of occupational asthma. The immunological mechanism is probably related to an IgE mediated mast cell allergy.
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PMID:Occupational asthma caused by exposure to neurospora in a plywood factory worker. 202 96

We conducted a series of experiments to determine if anticholinergics induce immediate cutaneous wheal-and-flare responses in normal volunteers. We performed intradermal skin testing in seven healthy volunteers (three atopic and four nonatopic) with 20 nmol of atropine. All subjects had an immediate wheal-and-flare response to atropine. To determine if this cutaneous response was due to anticholinergics in general, skin testing was also performed to scopolamine and ipratropium. These agents also produced immediate wheal-and-flare responses in all subjects, but they less potent than atropine. Pretreatment with antihistamines equivalently inhibited wheal-and-flare responses to both histamine and atropine, indicating a possible mast cell role. The potential role of M1, M2, and M3 muscarinic receptor subtypes was evaluated by use of the selective antagonists, pirenzepine (M1), 11[[2-1[(diethylamino)methyl]-1-piperidinyl]-acetyl]-5, 11-dihydro-6H-pyrido[2,3-b][1,4]benzodiazepine-6-one (AFDX-116) (M2), and 4-diphenylacetoxy-N-methylpiperidine (4-DAMP) (M3). Cutaneous wheal responses induced by pirenzepine and 4-DAMP were relatively equivalent and larger than responses induced by AFDX-116 at doses less than 200 nmol. At 200 nmol, all three muscarinic receptor subtype antagonists induced equivalent wheal formation. We then compared the cutaneous wheal responses to these specific muscarinic receptor antagonists based on their relative affinity for their respective muscarinic receptor subtype. This comparison suggested that M1 or M2, but not M3, muscarinic receptor subtypes may be important in anticholinergic-induced cutaneous wheal-and-flare responses. We propose that there may be an M1 or M2 muscarinic autoreceptor that inhibits the release of acetylcholine and other neurotransmitters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cutaneous responses to anticholinergics: evidence for muscarinic receptor subtype participation. 202 47

1. Systemic capsaicin treatment of the pig depletes the content of sensory neuropeptides (CGRP and tachykinins) in the airways mucosa and skin, without affecting sympathetic and parasympathetic nerves containing NPY and VIP, or the presence and appearance of inflammatory cells including mast cells. Acute capsaicin exposure caused release of sensory neuropeptides and catecholamines, and marked vasodilation in the airways and skin, without signs of plasma protein extravasation or bronchoconstriction. Capsaicin pretreatment effectively desensitizes against local challenges with capsaicin in the airways and skin, as revealed by the absence of vasodilatory responses 2 days later. 2. Cigarette smoke exposure induces marked vasodilatation, lasting for about 5 min in both the upper and lower airways, which seems not to be primarily caused by particulate matter or nicotine in the smoke. Except for a minor capsaicin-sensitive component in the nasal circulation, these responses probably do not involve neural activation, mast cell degranulation or prostaglandin formation. Rather, it is concluded that vapour phase components act on the vessels via unknown mechanisms. 3. Sensitization of pigs with s.c. injections of ascaris antigen was successful, resulting in typical wheal and flare reactions in the skin and bronchoconstriction after local challenge with antigen. The reactivity to ascaris is probably mediated by antibodies of the IgE isotype. 4. Histamine-containing mast cells and sensory neuropeptide-containing nerve fibers show close morphological association around blood vessels in the pig skin. Both alcian blue-positive mast cells and capsaicin-sensitive sensory nerves are present close to the pig airways epithelium. Sensory neuropeptide-containing nerves are also abundant around airways mucosal blood vessels, whereas the bronchial smooth muscle is sparsely innervated. 5. Allergen and histamine injections in the skin caused similar responses consisting of flare and protein extravasation. Allergen challenge in the airways induces marked vasodilatation lasting for 60-90 min in the pig bronchial and nasal circulations. Histamine seems to be important in the early phase (0-20 min) of these responses in the airways, while cyclooxygenase products (possibly PGD2) may be responsible for the longlasting component. A cyclo-oxygenase product is presumably also released from the lung into the circulation after bronchial allergen challenge and thereby induces a delayed, long-lasting nasal vasodilatation. Histamine may be the main bronchoconstrictor agent released in the immediate allergic reaction of the pig. 6. The flare, but not the protein extravasation reaction, to allergen and histamine injections in the skin, was inhibited by capsaicin pretreatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Airways vasodilatation in the immediate allergic reaction. Involvement of inflammatory mediators and sensory nerves. 203 38

Skin prick tests with allergen and histamine were performed on the volar aspect of the forearms in a double-blind, cross-over study with 40 mg of prednisolone and placebo in 16 pollen-allergic subjects. Skin biopsies were taken before any treatment and 15 min (group 1; n = 8) and 6 h (group 2; n = 8) after local challenge with allergen, corresponding to the timing of an early- and late-phase reaction. The specimens were used for the histological evaluation of mast cell and eosinophil density as well as for the determination of the histamine and protein content. The size of the induced weal and flare area as well as of any late-phase reaction was determined using digitized planimetry. The single dose of prednisolone, given 2 h prior to challenge, did not affect the size of the weal and flare response. Only 4 of the individuals developed a visible late-phase response. Eosinophils were virtually absent before allergen exposure, but were already present 15 min after allergen challenge, largely associated with the blood vessels, and were numerous at 6 h. There was, however, no relationship between eosinophil density and the presence or extent of any visual late phase. The mast cells/basophils showed a tendency to increase at the 6-hour determination. The infiltration of eosinophils was blocked by the glucocorticoid. This treatment also induced a difference in the mast cell density at the 6-hour determinations, associated with a similar difference in the histamine content of the biopsy specimens.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mast cells, tissue histamine and eosinophils in early- and late-phase skin reactions: effects of a single dose of prednisolone. 209 42

The wheal-and-flare response to intradermal autologous serum in chronic urticaria offers a model for study of the pathogenesis of the disorder. Serial biopsies of autologous serum induced wheals were performed in 5 chronic urticaria patients to assess the evolution of the cellular inflammatory response and to look for evidence of mast cell degranulation. Perivascular neutrophils and eosinophils were seen as early as 30 min, becoming more intense and diffuse over 2 h. T lymphocyte numbers were increased by 2 h, CD4+ cells outnumbering CD8+ cells at 24 h. By 48 h, the neutrophils were clearing, but eosinophils and lymphocytes persisted. The histology of compound 48/80-induced wheals was similar to serum-induced wheals, but there was little or no response to physiological saline (0.16 M). Stainable mast cells were reduced in compound 48/80- and serum-induced wheals when compared to saline skin tests. Mast cell granules appeared swollen and had lost their characteristic lamellar substructure on electron microscopy of a serum-induced wheal biopsied at 10 min. Eosinophil degranulation was also observed at 2 h. The resemblance of the inflammation to the late phase of IgE-mediated immediate hypersensitivity reactions in atopics supports the concept that a circulating factor causes mast cell degranulation in chronic urticaria and may be important in the pathogenesis of the disorder.
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PMID:The pathology of the autologous serum skin test response in chronic urticaria resembles IgE-mediated late-phase reactions. 209 45


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