Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Certain opioids release histamine from cutaneous mast cells to produce local wheal and flare responses and adverse hemodynamic effects. In vivo responses to opioids suggest that cutaneous responses result from the interaction of opioids with opioid receptors on human mast cells. There are no data evaluating or comparing the opioids currently used in anesthesia. Volunteers were injected intradermally with different opioids as well as with naloxone and antihistamines to evaluate their effects on cutaneous mast cell reactivity and cutaneous vascular responses. Fentanyl and morphine produced concentration-dependent wheal and flare responses in the range of 5 X 10(-6) M to 1.5 X 10(-3) M. Volunteers were then tested intradermally with different opioids and histamine at a 5 X 10(-4) M concentration to determine their relative cutaneous effects. Morphine, meperidine, fentanyl, and sufentanil produced both wheal and flare responses that were significantly greater than those due to saline (P less than 0.05). Naloxone, alfentanil, and nalbuphine did not produce significant wheal or flare responses. Butorphenol was followed by a significant wheal but no flare. Naloxone attentuated cutaneous wheal and flare responses to fentanyl and the flare response to morphine. Intradermal antihistamines (diphenhydramine and cimetidine) produced significant wheal and flare responses. Electron micrographs of biopsies from fentanyl-induced wheals demonstrated normal mast cell architecture with no evidence of mast cell degranulation. Opioid effects on wheal and flare responses and mast cell degranulation appear independent of opioid analgesic potency. Opioids produce cutaneous vascular responses dependent on both histamine release from mast cells and direct effects on the vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Wheal and flare responses to opioids in humans. 247 Feb 72

Antihuman IgE is often used to study basophil- and mast cell-mediator release in vitro but is infrequently used in vivo. To evaluate in vivo skin reactivity to anti-IgE, an affinity-purified rabbit F(ab')2 fragment of antihuman IgE was injected intradermally in 22 nonallergic and 27 allergic subjects. All 49 subjects (including a subject with less than 1 ng/ml of total serum IgE) had positive immediate cutaneous reactions to anti-IgE. Although total serum IgE level was weakly correlated (r = -0.51; p less than 0.005) with in vivo skin reactivity to anti-IgE for the entire population, allergic subjects did not have significantly increased skin reactivity compared to nonallergic subjects (p = 0.18), despite having higher total serum IgE levels (p less than 0.002). A late-phase cutaneous response (LPR) to anti-IgE occurred in 60% of the allergic and in 50% of the nonallergic subjects. Subjects with an LPR required approximately tenfold higher concentrations of anti-IgE to produce an immediate wheal of 10 mm compared to subjects who did not develop an LPR (p = 0.02), suggesting that the concentration of the stimulus injected is more important for the development of a LPR than the size of the immediate cutaneous response. Skin reactivity to codeine phosphate (a non-IgE-dependent secretagogue) was correlated with skin reactivity to anti-IgE (r = 0.47; p less than 0.05), suggesting that in vivo skin mast cell degranulation is partially a function of mast cell releasability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rabbit F(ab')2 antihuman IgE is a universal skin test reagent in the evaluation of skin mast cell degranulation in vivo. 247 17

Adenosine 5'-monophosphate (AMP) in increasing concentrations, and saline solutions of corresponding tonicity, were injected intradermally in seven atopic and seven normal subjects. Skin wheal-and-flare responses were elicited in a dose-dependent fashion in all subjects, and no difference was found between responses produced by AMP and responses produced by saline of corresponding tonicity. Also, no difference in response to AMP and saline was found between atopic and nonatopic subjects. We further investigated, in seven atopic subjects, whether the skin wheal-and-flare response to the single, highest dose of AMP, saline, and histamine could be inhibited by preadministration of 180 mg of terfenadine, a potent H1 antagonist. A significant inhibition of the wheal-and-flare response to histamine and no significant inhibition to AMP were found. There was a significant inhibition of the flare response caused by hypertonic saline but no inhibition of the wheal response. We interpret these findings as indicating that AMP does not specifically lead to mast cell degranulation in the skin and that there are functional differences between cutaneous and lung mast cells. The observation that terfenadine significantly inhibited the flare response to hypertonic saline suggests that this stimulus produced histamine release.
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PMID:Wheal-and-flare responses to intradermally injected adenosine 5'-monophosphate, hypertonic saline, and histamine: comparison of atopic and nonatopic subjects. 250 63

Previous studies have shown that pretreatment of skin with beta 2-adrenoceptor stimulants antagonizes anti-human IgE elicited wheal and flare reactions in atopic and non-atopic subjects. This experimental system was employed to further study the hypothesis that atopic disease and bronchial asthma unrelated to atopy might be associated with a beta-adrenoceptor defect. Eight patients with extrinsic and 10 patients with intrinsic asthma deprived of oral bronchodilator treatment and corticosteroids for at least a week, and in a clinically stable condition, 10 patients with extrinsic rhinitis and on no treatment, as well as age and sex matched healthy control subjects showed almost identical dose-response relations for the inhibitory effect of intradermally injected terbutaline (0.25-100 ng), on anti-IgE elicited skin reactions. In four asthmatic patients the inhibitory effect of terbutaline did not change following a treatment period with oral terbutaline and theophylline. The data do not support the presence of a cutaneous mast cell beta 2-adrenoceptor defect in patients with atopy or bronchial asthma unrelated to atopy.
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PMID:Equivalent inhibition by terbutaline of anti-human IgE skin responses in atopic and non-atopic subjects. 257 97

The inhibitory effects of topical glucocorticosteroid treatment on the immediate dermal allergic reaction were studied in 10 patients in a double, randomized, placebo-controlled fashion. The aim was to study whether a prolongation of the treatment time would enhance the inhibitory effect beyond the 30-40% reduction previously reported after 1 week of treatment, and whether any changes in skin reactivity were accompanied by changes in the level of mast cells or histamine at the challenge site. Allergen and histamine skin-prick tests were performed on both forearms before the start of the study and after 2 and 4 weeks of treatment with placebo cream on one forearm and with 0.05% clobetasol-17-propionate cream on the other. Punch biopsies from the skin treated actively and with placebo were taken after 4 weeks in eight of the patients. The specimens were used for the light-microscopic evaluation of mast cell density and for the measurement of histamine and protein content. After 4 weeks of treatment we found a reduction in the allergen-induced weal (72%; P less than 0.001) and flare (62%; P less than 0.05) response. There was also a minor reduction in the histamine-induced weal (38%; P less than 0.05) but not the flare response, suggesting that the glucocorticoid treatment induced a reduced mediator release at allergen challenge. This could be partially explained by the finding of a reduction in the number of detectable skin mast cells (85%; from 0.78 to 0.11 mast cells per unit area) and in the histamine content of the skin as related to the tissue wet weight (36%; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prolonged treatment with topical glucocorticoids results in an inhibition of the allergen-induced weal-and-flare response and a reduction in skin mast cell numbers and histamine content. 264 13

Forty-one subjects with dermographia were studied for a 4-week period. Twenty subjects received ketotifen therapy, the other 21 received chlorpheniramine (H1) for 2 weeks, and then chlorpheniramine plus cimetidine (H1 + H2). Both groups had significant suppression of dermographia and skin wheals caused by dextromethorphan and histamine after 2 weeks. The inhibition by ketotifen of dermographia, histamine wheal, and the dextromethorphan wheal increased from week 2 to week 4. During the first 2 weeks, ketotifen's activity was comparable to chlorpheniramine. Ketotifen's activity increased during the second 2 study weeks to match the additional chlorpheniramine. These results suggest that ketotifen may have additional pharmacologic activities besides H1 antagonism, including possible inhibition of mast cell mediator release. As a consequence, cutaneous vascular hyperresponsiveness may decrease. Ketotifen appears promising as treatment for allergic skin disorders.
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PMID:Inhibition of dermographia, histamine, and dextromethorphan skin tests by ketotifen. A possible effect on cutaneous vascular response to mediators. 277 2

Theophylline and enprofylline have been demonstrated to reduce mast cell-mediator release, inhibit polymorphonuclear leukocyte activation, and have been reported to reduce the late bronchial response to antigen. The effects of theophylline and enprofylline on the late cutaneous response (LCR) to compound 48/80 and antigen were studied in 29 patients enrolled in a placebo-controlled, double-blind study of the effect of the xanthines in mild asthma. Skin testing to a common environment allergen and compound 48/80 was performed during a baseline period and in the second phase of the study after stable drug levels were achieved, at least 6 weeks later. During baseline, the mean immediate wheal diameter (IWD) with antigen was 15.7 mm +/- 0.5, resulting in 27/29 LCRs with a mean wheal diameter of 37.1 mm +/- 5.2. The mean IWD with compound 48/80 was 16.1 mm +/- 0.7, resulting in 26/29 LCRs with a mean wheal diameter of 19.6 mm +/- 2.8. Repeat skin testing during treatment revealed no statistically significant changes in the LCR elicited by antigen or 48/80 in any of the treatment groups. There was little correlation between the size of the immediate wheal produced by antigen or 48/80 and the resulting size of the late response (r = 0.174 to 0.519). However, for the same IWD, the resulting late response was smaller with 48/80 than with antigen (p = 0.003). We conclude that (1) theophylline and enprofylline have no effect on the LCR to 48/80 and antigen and (2) for equivalent immediate wheal sizes, the resulting late response is smaller with 48/80 than with antigen.
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PMID:The effect of theophylline and enprofylline on the late cutaneous response to antigen and compound 48/80. 291 85

It has been suggested that patients with recurrent, unexplained anaphylaxis may be more responsive, and patients with systemic mastocytosis, less responsive, to mast cell-derived mediators, including histamine, compared to normal subjects. This would help explain why patients with recurrent, unexplained anaphylaxis have an anaphylactic response and, conversely, why patients with systemic mastocytosis can tolerate high levels of plasma histamine. To test this hypothesis, intradermal titrations (0.02 ml of solution from 1 ng/ml to 2 micrograms/ml) of histamine and morphine sulfate (MS) (10 ng/ml to 10 micrograms/ml) were administered to normal volunteers (N = 15), patients with recurrent, unexplained anaphylaxis (N = 10), and patients with systemic mastocytosis (N = 18). Antihistamines were stopped at least 72 hours before the study. Resultant areas of wheal and flare were determined with a computerized morphometric system. Comparison of any two given means at each dose of histamine or morphine with the two-sample Student's t test with Bonferroni inequality demonstrated no significant differences (p greater than 0.05) among the three groups. The median amount of MS or histamine required to produce a half-maximal response was compared for equality. None of the differences observed reached statistical significance, in agreement with the similarity of the dose-response curves. An analysis of the correlation between response to MS and to histamine in individual subjects revealed the responses to be significantly correlated in all cases, with the exception of wheal in patients with recurrent, unexplained anaphylaxis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of the wheal-and-flare reactions that follow the intradermal injection of histamine and morphine in adults with recurrent, unexplained anaphylaxis and systemic mastocytosis. 292 81

Leukotrienes are synthesised from arachidonic acid via the 5-lipoxygenase pathway in neutrophils, eosinophils, monocytes/macrophages, basophils and certain mast cell populations. Their synthesis is closely regulated by several known factors and the cells which contain 5-lipoxygenase do not all possess the capability to synthesise all of the leukotrienes. Neutrophils produce leukotriene B4, which attracts other neutrophils, whereas the leukotriene C4, produced by eosinophils, increases the contractile activity of smooth muscle. Monocytes/macrophages are able to produce both of these leukotrienes. Receptor sites for leukotriene B4 have been identified on monocytes and neutrophils and receptors for leukotriene D4, a cleavage product of leukotriene C4, have been defined in pulmonary tissue. In animals, sulphidopeptide leukotrienes have been shown to cause potent vasoconstriction resulting in increased blood pressure and increased vascular permeability leading to hypovolaemia. These leukotrienes also depress renal (in animals) and pulmonary (in animals and humans) function, the latter probably as a result of effects on peripheral rather than central airways. In patients with mild asthma, however, there is no differential activity of this type. The sulphidopeptide leukotrienes caused wheal and flare when administered intradermally in healthy volunteers, which was of considerably longer duration than that induced by prostaglandin D2. Conversely, leukotriene B4 caused accumulation of neutrophils in the absence of wheal and flare. Studies into the effects of dietary fish oil showed that 2 constituents, docosahexanoic acid and eicosapentaenoic acid (EPA), inhibit the conversion of arachidonic acid by cyclo-oxygenase, but not by 5-lipoxygenase. Furthermore, 5-lipoxygenase converts EPA to a pentene series of leukotrienes and the sulphidopeptide derivatives possess similar activity to their tetrameric counterparts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of arachidonic acid metabolites in local and systemic inflammatory processes. 303 59

The effect of nifedipine on subjective symptoms and objective dermographometer induced whealing was assessed independently in two double-blind cross-over trials in which active drug or placebo were taken for 2 weeks. The lower dose study used nifedipine 5 mg 3 times daily and gave rise to symptomatic improvement as assessed by diary card and visual analogue scale in 5 of 11 patients. This was not statistically significant and was not accompanied by a reduction in dermographometer-induced wheal and flare responses except at highest pressures. In a separate study 7 patients were treated with nifedipine 10 mg 3 times daily. No change in whealing occurred, 3 patients' symptoms became worse and only 1 showed symptomatic improvement on nifedipine. Side effects were frequent at this dose. The reasons for the unfavourable response despite in vitro evidence for inhibition of mast cell degranulation by this drug are discussed.
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PMID:Calcium antagonist in the treatment of symptomatic dermographism. Low-dose and high-dose studies with nifedipine. 307 23


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