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)

We investigated itch-associated responses (scratching) to mosquito bites and the role of histamine and mast cells in mosquito-induced itching in mice. Although the first bites of mosquito Aedes albopictus did not increase scratching, repeated bites increased scratching. The response was not diminished even after an interval of 2 months. Similarly, repeated intradermal (i.d.) injections of salivary gland extract (SGE) from Aedes albopictus increased scratching after SGE injection itself and mosquito bites. The scratching peaked within 10 min and almost subsided by 60 min. The opioid antagonist naloxone (1 mg/kg, s.c.) inhibited scratching following SGE injection. Although the non-sedative H1-histamine-receptor antagonist terfenadine (30 mg/kg, p.o.) significantly suppressed scratching induced by histamine (100 nmol/site, i.d.) in either naive or mosquito-sensitized mice, it did not affect mosquito-induced scratching in mosquito-sensitized mice. Repeated injections of SGE increased scratching in mast cell-deficient (WBB6F1-W/Wv) mice as well as in normal (WBB6F1-+/+) littermates. Repeated exposure to mosquito bites roughly doubled serum concentrations of total IgE and IgG1, but not IgG2a. Repeated injections of SGE markedly increased plasma extravasation induced by mosquito bites and such an increase was almost completely suppressed by terfenadine (30 mg/kg, p.o.). The results show the presence of histamine-mediated and histamine-independent mechanisms in cutaneous itching and suggest that histamine probably released from mast cells does not play an important role in itching in immediate allergic reaction. Our murine model of mosquito itching may be useful for studying the mechanisms of immediate allergic itching.
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PMID:Roles of mast cells and histamine in mosquito bite-induced allergic itch-associated responses in mice. 1143 Apr 78

The mode of action of intranasal corticosteroids (INCS) is complex. It is not known whether INCS penetrate the nasal mucosa or act on target cells; however, their low systemic activity supports the concept of local action on nasal mucosa. This local effect can nonetheless influence a variety of inflammatory cells and their mediators such as epithelial cells, lymphocytes, basophils, mast cells, and Langerhans cells. Corticosteroid-induced inhibition of immunoglobulin E-dependent release of histamine is a possible but unproven mode of action. Epithelial cells are an important target for corticosteroids, and INCS concentration is high at the epithelial surface. INCS may combine with the corticosteroid receptors in epithelial cells, which are then expelled into the airway lumen together with the dead epithelial cells or migrating inflammatory cells. A reduced influx of mediator cells may explain some of the effects of INCS on rhinitis symptoms, but it cannot explain all of the effects because INCS also reduce the early-phase sneezing and rhinorrhea after an allergen challenge outside the pollen season. In this situation, the number of surface mast cells/basophils is very low, as it is in the absence of allergic rhinitis. The mechanism by which INCS treatment of allergic rhinitis reduces itching, sneezing, and rhinorrhea, the characteristic symptoms of an early-phase response involving mast cell release of histamine, remains to be determined. Studies should be conducted to characterize the broad range of mechanisms by which INCS produce their therapeutic effects in allergic rhinitis.
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PMID:Mode of action of intranasal corticosteroids. 1144 2

The pathogenesis of uraemic pruritus is unclear, although there is some evidence that an increased number of skin-infiltrating mast cells may play a role. Ultraviolet B reduces itchy sensation of uraemic patients by leading to depletion of cutaneous mast cells. This study presents data that both broad-band and narrow-band ultraviolet B irradiation are able to induce apoptosis in transformed mast cells (murine mastocytoma cell line P815) in a dose-dependent manner at a time point of 24 hours. The positive apoptotic rates were as follows: sham-exposed cells (controls) -- 13.3% +/- 0.6%; with broad-band ultraviolet B irradiation -24.5% +/- 1.1% with 10mJ/cm(2), 57.9% +/- 4.6% with 20mJ/cm(2) and 70.9% +/- 4.5% with 30mJ/cm(2); with narrow-band ultraviolet B irradiation -- 29.6% +/- 2.3% with 100mJ/cm(2), 57.3% +/- 4.1% with 200mJ/cm(2) and 81.5% +/- 1.9% with 300mJ/cm(2). The difference between the number of apoptotic cells in all groups of ultraviolet B-irradiated cells and sham-exposed cells was highly significant (P<0.001). Based on these findings, it is hypothesized that ultraviolet B induced mast cell apoptosis could be an important factor in phototherapy for the diseases dependent on increased number of cutaneous mast cells, including uraemic pruritus.
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PMID:Ultraviolet B induces mast cell apoptosis: a hypothetical mechanism of ultraviolet B treatment for uraemic pruritus. 1181 97

Anaphylaxis is an acute fatal or potentially fatal hypersensitivity reaction. Anaphylaxis represent a clinical diagnosis based on history and physical examination and includes symptoms of airway obstruction, generalized skin reactions, particularly flushing, itching, urticaria, angioedema cardiovascular symptoms including hypotension and gastrointestinal symptoms. These symptoms result from the action of mast cell mediators, especially histamine and lipid mediators such as leukotrienes and platelet activating factor on shock tissue. The shock tissue includes blood vessels, mucous glands, smooth muscle, and nerve endings. Anaphylaxis follows the typical immediate hypersensitivity time course, with a reaction beginning within minutes of antigen exposure. A late-phase reaction hours after the initial reaction may occur. Mast cell mediator release can be triggered by both IgE and non--IgE-mediated factors. Therefore, anaphylaxis may be termed anaphylaxis (IgE mediated) or anaphylactoid (non--IgE mediated). The most common IgE-mediated triggers are drugs, typically penicillin or other beta-lactam antibiotics, foods, most commonly nuts, peanuts, fish and shellfish, or hymenoptera stings. Non-IgE-mediated causes include factors causing marked complement activation such as plasma proteins or compounds which act directly on the mast cell membrane, such as vancomycin, quinolone antibiotics, or radiographic contrast media. The pathophysiology of some trigger factors, such as aspirin, remains unclear. Therapy of anaphylaxis revolves around patient education, avoidance, desensitization or pharmacologic pretreatment when agents causing anaphylaxis need to be readministered, and early recognition and prompt therapy of reactions should they occur.
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PMID:Anaphylaxis and Anaphylactoid Reactions: Diagnosis and Management. 1186 83

The pathogenesis of allergic rhinitis can be better appreciated by understanding the numerous protective mechanisms available for mucosal defense. The system of TH2 lymphocytes, IgE production, mast cell degranulation, eosinophil infiltration, and resident cell responses are central to our understanding and treatment of allergic rhinitis. Histamine remains preeminent in causing the cardinal symptoms of the immediate allergic reaction: itching, watery discharge, and nasal swelling. Recruitment and activation mechanisms responsible for the late-phase allergic response are also reviewed.
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PMID:Mechanisms of allergic rhinitis. 1189 38

Patients with systemic mastocytosis present symptoms related to the tissue response to the release of mediators from mast cells and to the local mast cell burden. Such patients often have a history of chronic and acute mediator-related symptoms. Most patients have indolent disease with a good prognosis and a normal life span. Symptoms can include pruritus, flushing, syncope, gastric distress, nausea and vomiting, diarrhea, bone pain and neuropsychiatric symptoms, most of which are controlled by medication. Because there is no current cure for mastocytosis, successful therapeutic interventions rely on the recognition of mediator-related symptoms and their treatment, and established intervention approaches for the relatively uncommon leukemic concomitants. Efforts to link a particular mast cell-derived mediator to some aspect of the symptom complex depend on the known actions of the mediator and the efficacy of target-based interventions.
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PMID:Mastocytosis: mediator-related signs and symptoms. 1191 27

The present study was conducted to establish a new mouse model of dry skin pruritus. The rostral back was treated daily with cutaneous application of acetone/ether (1:1) mixture (AE), water following AE (AEW), 1% sodium lauryl sulfate (SLS) or tape stripping (TS). On the day after 5-day treatment, although all four treatments significantly decreased stratum corneum (SC) hydration and increased transepidermal water loss (TEWL), only AEW treatment significantly increased spontaneous scratching. An increase in the frequency of TS produced the marked increase of TEWL, without significant effects on SC hydration and spontaneous scratching. In AEW-treated mice, changes in SC hydration and TEWL were marked in the initial 2-day period, while spontaneous scratching increased gradually from 3 days after starting the treatment. The degranulation of cutaneous mast cells was increased by SLS treatment but not by other treatments. There was no apparent difference in AEW-induced spontaneous scratching between mast cell-deficient mice (WBB6F1-W/Wv) and normal littermates (WBB6F1-+/+). Opioid antagonists, naloxone and naltrexone, (1 mg/kg, subcutaneously) significantly suppressed spontaneous scratching in AEW-treated mice. It is suggested that spontaneous scratching of AEW-treated mice is an itch-related response and a useful model for studying the mechanisms of dry skin pruritus.
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PMID:Itch-associated response induced by experimental dry skin in mice. 1194 83

The term mastocytosis denotes a heterogeneous group of rare hematological disorders characterized by abnormal accumulation of mast cells. While cutaneous mastocytosis is relatively frequent mast cell leukemia belongs to the rarest forms of human leukemia. In the following we present the case of an aleukemic mast cell leukemia and shall discuss the revised classification of mastocytosis based on the "Year 2000 Working Conference on Mastocytosis" held in Vienna, Austria. A 48 year-old caucasian man presented with a four-week history of diarrhea, obstipation, vomiting, rash, and mild fever. Clinical inspection revealed a disseminated itching rash and a mild hepatomegaly. Red and white blood cell counts were within the normal range. Levels of the alkaline phosphatase and serum histamine were significantly increased. There was no splenomegaly or lymphadenopathy. Cytologic and histologic investigation of the bone marrow revealed a marked increase in atypical mast cells. Since only a few circulating mast cells could be detected in a cytospin preparation of the blood, the diagnosis of an aleukemic mast cell leukemia was established. About four weeks after the diagnosis had been established, the patient died with signs of a hemorrhagic shock due to a massive gastrointestinal bleeding. Autopsy revealed widespread mast cell infiltration of bone marrow, spleen, liver and lungs, but also a small, deeply penetrating, non-specific duodenal ulcer. In conclusion, despite of presentation with signs of a primary gastrointestinal disorder, the patient was found to suffer from an exceedingly rare aleukemic mast cell leukemia ("malignant mastocytosis") and died after a total duration of the disease of only about three months.
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PMID:[Aleukemic mast cell leukemia (formerly: "malignant mastocytosis"): an extremely rare form of leukemia. A case report and simultaneously a contribution to revised classification of mastocytosis]. 1223 4

Histamine release from mast cells is a primary mediator of rhinorrhea, nasal mucosal swelling, increased secretion, sneezing, pruritus and congestion that occur in allergic rhinitis. It is well known that histamine H(1) receptor antagonists inhibit the itch and rhinorhea, but do not block the allergic nasal congestion. A growing body of evidence shows that in addition to histamine H(1) receptors, activation of H(3) receptors may contribute to the procongestant nasal actions of histamine. Activation of the prejunctional histamine H(3) receptor modulates sympathetic control of nasal vascular tone and resistance. The present study was conducted to further characterize the role of histamine H(3) receptors on neurogenic sympathetic vascular contractile responses in isolated porcine nasal turbinate mucosa. We presently found that the histamine H(3) receptor agonist, (R)-alpha-methylhistamine (10-1000 nM), inhibited electrical field stimulation-induced sympathetic vasomotor contractions in a concentration-dependent fashion. Pretreatment with either of the selective histamine H(3) receptor antagonists, thioperamide and clobenpropit, blocked the sympathoinhibitory effect of (R)-alpha-methylhistamine in porcine turbinate mucosa. The effect of compound 48/80, an agent that elicits the release of endogenous histamine from mast cells on nasal sympathetic contractile responses, was also tested. The action of compound 48/80 to release mast cell-derived histamine in the nose mimics many of the nasal responses associated with allergic rhinitis, extravascular leakage and decreased nasal patency. We presently found that compound 48/80 also inhibited the electrical field stimulation-induced sympathetic response. Pretreatment with the H(3) receptor antagonist clobenpropit blocked the sympathoinhibitory action of compound 48/80 on sympathetic contractile responses in nasal mucosa. Taken together, these studies indicate that histamine H(3) receptors modulate vascular contractile responses by inhibition of noradrenaline release from sympathetic nerve terminals in nasal mucosa. It is further suggested that histamine H(3) receptors may play a role in the regulation of vascular tone and nasal patency in allergic nasal congestive disease.
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PMID:Histamine H3 receptor activation inhibits neurogenic sympathetic vasoconstriction in porcine nasal mucosa. 1235 75

We examined the scratch (itch) inducing effect of 1,8-cineole (cineole), a monoterpene oxide present in many plant essential oils and the possible role of mast cells in the response. Subcutaneous injection of cineole (10, 20 and 40 microl/site) or the mast cell degranulating agent, compound 48/80 (25, 50 and 100 microg/site) into the rostral back of mice induced a scratching behavior. This response of cineole as well as that of 48/80 was markedly suppressed in mice subjected to mast cell desensitization by repeated injections of 48/80. The cineole-induced scratching was also significantly diminished in animals pretreated with diphenhydramine, the histamine H1-receptor antagonist or cyproheptadine, the dual histamine/serotonin-receptor antagonist. Furthermore, the scratch-inducing effect of cineole was greatly reduced in mice that received the opioid antagonist naloxone or the selective adenosine A1-receptor agonist, N6-cyclopentyladenosine (CPA), but not the more selective adenosine A2-receptor agonist, 5'-N-ethylcarboxamidoadenosine (NECA). The data suggest a likely role for mast cells in cineole-induced scratching behavior of mice, possibly involving adenosinergic and opioidergic mechanisms.
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PMID:Possible role of mast cells in cineole-induced scratching behavior in mice. 1238 8


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