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

Mast cells are involved in allergic reactions where they secrete numerous mediators in response to immunoglobulin E and antigen. However, they have recently been implicated in neuroinflammatory conditions with a higher prevalence in women, and there have been clinical reports of progesterone anaphylaxis. When tested on purified rat peritoneal mast cells, progesterone alone stimulated release only of 5-hydroxytryptamine (serotonin) in a dose- and time-dependent manner. Serotonin release by progesterone was exceptional because it was not accompanied by histamine release or degranulation and was either augmented or unaffected by drugs which inhibit secretion induced by the classic mast cell secretagogue, compound 48/80. These findings indicate that mast cells are capable of selective serotonin secretion, previously shown only after pretreatment with certain tricyclic drugs, and may be involved in neuroendocrine syndromes.
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PMID:Progesterone triggers selective mast cell secretion of 5-hydroxytryptamine. 209 39

Mast cell-competent mice, sensitized to lysozyme, were examined for their mast cell and anaphylactic responses to determine whether anaphylactic shock could occur independent of mast cell participation. Tissues (cremaster muscle, subdermal connective tissue and mesentery), taken a short time after intravenous antigenic challenge, showed no evidence of mast cell degranulation above control tissues. Data obtained from a quantitative comparison of the onset and increase in local and systemic anaphylactic and mast cell sensitivities to the antigen provide strong support for the view that mast cells are not the major effector cells for systemic anaphylaxis in mice. The significant increase in blood pressure that occurred immediately after infusion with the antigen also indicates that other cells within the blood stream are involved.
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PMID:Lack of correlation between mast cell response and active anaphylaxis in mice. 209 48

The ocular late-phase reaction (LPR) is a mast cell-dependent, delayed inflammatory reaction developing 4-12 h after the early-phase reaction (EPR). We developed a passive IgG1 antibody-dependent guinea pig model that clinically reproduced the biphasic reaction of ocular EPR and LPR. An EPR was observed in all animals; a biphasic, multiphasic or prolonged inflammation was observed in the animals maintained for 9 and 24 h. The substantia propria of eyes undergoing EPR (0.5 h) showed intense edema, mast cell degranulation (88%), and 4-fold increase in eosinophils. At 9 h, the neutrophils and eosinophils had increased 11- and 25-fold, respectively. The number of basophils and lymphocytes was significantly increased compared to the controls (p less than 0.05). Of the mast cells, 45% were degranulated compared with 19% for controls. Cellular reactions had subsided by 24 h. Conjunctival epithelium also accumulated inflammatory cells as did the stroma of the lid skin. These histologic changes in ocular tissues undergoing anaphylaxis demonstrated that mast cell degranulation was most severe in the early phase, whereas neutrophil, eosinophil, and basophil accumulation was most marked in the late phase.
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PMID:Histology of ocular late-phase reaction in guinea pigs passively sensitized with IgG1 antibodies. 212 38

Tryptase, a mediator secreted by human mast cells during immediate reactions, has demonstrated effects on several pathways in vitro. This enzyme can rapidly inactivate fibrinogen and, as a complex with heparin, may prevent coagulation that may otherwise occur when plasma enters tissues at sites of immediate reactions. Tryptase may also activate prostromelysin, which in turn activates latent collagenase. When canine pulmonary smooth muscle is incubated with canine tryptase, the contractile response to histamine is increased. Tryptase, quantifiable in complex biologic fluids by immunoassay, can serve as a specific indicator of mast cell involvement in certain clinical settings. For example, after bee sting--induced anaphylaxis, tryptase levels in the blood peak at approximately 1 hour, then decline with a half-life of approximately 2 hours. Additionally, elevated tryptase levels in bronchoalveolar lavage fluid of asymptomatic, atopic persons with asthma suggest ongoing mast cell activation, which may relate to adenosine hyperresponsiveness and a persistence of bronchial hyperreactivity. Tryptase levels in bronchial lavage fluid of atopic patients with asthma rise markedly after endobronchial allergen challenge but not after an exercise challenge, suggesting a lack of mast cell involvement in the latter condition.
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PMID:Tryptase, a mediator of human mast cells. 222 22

Homocytotropic antibody was stimulated in animals by administering protein antigens in a vaccine with B. pertussis adjuvant. The titers of the allergic antibody responses were judged by passive cutaneous anaphylaxis reactions. Sera or globulin fractions containing high titers of antibody activity were injected into the knee joints of experimental animals. After sufficient delay for unfixed proteins to be cleared from the knee joints, animals were challenged intravenously with the corresponding antigen. The resultant local reaction of swelling and warmth (passive synovial anaphylaxis) was judged visually and by scanning procedures. Histological studies showed evidence of mast cell degranulation concurrent with synovial reaction.
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PMID:Joint inflammation provoked by a local synovial allergic reaction. 225 85

Dinitrophenyl (DNP) derivatives of various molecular weights were tested for their ability to elicit ocular anaphylaxis after topical application to the eye of immunized animals. Adult male Sprague-Dawley rats were immunized by intraperitoneal injection of DNP-Ascaris suum extracts and alum and were then skin-tested with DNP-bovine serum albumin on day 13 post-immunization to assess their sensitivity to the DNP hapten. On day 14, animals were challenged topically with DNP derivatives in one eye; PBS was applied to the contralateral, control eye. Animals were evaluated clinically, and ocular tissues were processed for histologic evaluation. The compounds used for topical ocular challenge included the DNP derivative of egg albumin (MW 43,500 D), soybean trypsin inhibitor (MW 20,080 D), insulin (MW 5733 D), B-chain insulin (MW 3496 D), and lysine (MW 478 D). Only di-DNP-lysine elicited clinical signs of redness, edema, and tearing and histologic evidence of mast cell degranulation. None of the other compounds, tested in solutions of either equal numbers of milligram per milliliter or equimolar concentrations, elicited ocular anaphylaxis after topical application. A compound of low molecular weight, less than 3496, is needed to elicit ocular anaphylaxis when applied topically.
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PMID:Penetrating the conjunctival barrier. The role of molecular weight. 230 28

Lesional (n = 15) and non-lesional (n = 10) skin of subjects with mastocytosis was analysed for the distribution and concentration of trypase positive, chymase negative mast cells (MCT) and tryptase positive, chymase positive mast cells (MCTC) cells and compared to normal skin (n = 23) and non-lesional skin of subjects with unexplained anaphylaxis or flushing episodes (n = 6). Skin biopsies were fixed in Carnoy's fluid and subjected to double immunohistochemical staining with biotinylated mouse monoclonal anti-chymase antibody followed by alkaline phosphatase-conjugated mouse monoclonal anti-tryptase antibody. MCTC cells were the only type of mast cells seen in all specimens analysed and in each case were more numerous in superficial compared to deep regions of dermis. The concentration (mean +/- s.d.) of mast cells in the superficial dermis of mastocytosis lesions (40 985 +/- 21 772 mast cells/mm3) was significantly increased over that in corresponding areas of non-lesional skin from subjects with mastocytosis (7178 +/- 3607 mast cells/mm3), skin from subjects with idiopathic anaphylaxis or flushing episodes (6974 +/- 3873 mast cells/mm3) and normal skin (7347 +/- 2973 mast cells/mm3). The exclusive presence of MCTC cells in skin lesions of mastocytosis which are characterized by non-malignant hyperplasia of mast cells suggests involvement of local tissue factors in mast cell recruitment and differentiation.
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PMID:Mast cells in cutaneous mastocytosis: accumulation of the MCTC type. 231 Sep 82

The normal skin and other tissues of adult genetically mast cell-deficient WBB6F1-W/Wv or WCB6F1-Sl/Sld mice contain less than 1.0% the number of mast cells present in the corresponding tissues of the congenic normal (+/+) mice. We previously reported that mature dermal mast cells developed locally in the skin of W/Wv, but not Sl/Sld, mice at sites of chronic idiopathic dermatitis. We now report that the repeated application of phorbol 12-myristate 13-acetate (PMA) to the ear skin of either W/Wv or +/+ mice induces both dermatitis and a striking and dose-dependent increase in the number of dermal mast cells. The number of dermal mast cells at sites treated for 6 weeks with 5 micrograms PMA, three times per week, was 39 +/- 7/mm2 and 305 +/- 34/mm2 for W/Wv and +/+ mice, respectively; the corresponding values for vehicle-treated skin were 1.5 +/- 1.0/mm2 and 145 +/- 8/mm2, respectively. The PMA-induced dermal mast cells in W/Wv mice appeared mature by morphology, stained with the heparin-binding fluorescent dye, berberine sulfate, and were competent to express IgE-dependent passive cutaneous anaphylaxis responses. The development of mast cells was a local, not systemic, effect of PMA treatment. PMA treatment also induced dermatitis in both WCB6F1-Sl/Sld and +/+ mice, but was associated with increased numbers of dermal mast cells only in the WCB6F1(-)+/+ mice. PMA treatment had no detectable effect on the ability of bone marrow-derived cultured mast cells to survive in the skin of Sl/Sld mice. These findings establish a convenient model system for analyzing factors associated with the development of endogenous populations of mast cells in genetically mast cell-deficient W/Wv mice.
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PMID:Phorbol 12-myristate 13-acetate-induced development of functionally active mast cells in W/Wv but not Sl/Sld genetically mast cell-deficient mice. 232 15

The present study was made on an experimental animal model of a death from anaphylaxis, in which postmortem changes in levels of histamine and 1-methylhistamine, in whole blood were measured. Instead of the usual immunological method administering compound 48/80, a degranulating agent of mast cell and the effect closely resembling the immuno-reaction, resulted in reliable death in a short time. The animals that died rapidly after the injection of compound 48/80, were found to have large increases in levels of histamine and 1-methylhistamine soon after the administration. These results were similar to the results of injecting histamine exogenously. On the other hand, the animals that died after a longer time showed no increases in levels of those amines within about 24 h, but 24 hours after death histamine levels were only increased tremendously without rise in 1-MHA levels. These phenomena closely resembled those in the control animals that were treated with overdoses of Nembutal.
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PMID:An experimental model of death from anaphylactic shock with compound 48/80 and postmortem changes in levels of histamine in blood. 233 30

The possible development of type-1 hypersensitivity reactions in the abomasal mucosa caused by soluble L3 products of Ostertagia ostertagi was studied in 4-month-old calves sensitized by repeated exposure to L3 over a 50-day period followed by anthelmintic treatment. Four groups each of 4 calves were used. Group 1 served as nonsensitized controls and group 2 as sensitized controls, group 3 was challenge exposed at 2-week intervals beginning at week 10 with a soluble L3 product (OAG), and group 4 was challenge exposed at 2-week intervals with an oral dose of L3, followed by anthelmintic treatment 3 days later. All calves infected with L3 became sensitized, as indicated by a positive reaction to an intradermal skin test. However, a passive cutaneous anaphylaxis was only partly effective in indicating the presence of homocytotropic antibody in the infected calves. Sensitized calves had significantly (P less than 0.05) higher eosinophil counts and plasma pepsinogen values for the entire 14 weeks than uninfected controls. Globule leukocyte and mast cell counts from the abomasal mucosa were also significantly (P less than 0.05) higher. Studies for possible immunomodulation revealed that lymphocyte counts decreased between every 2-week challenge-exposure period for groups-3 and -4 calves. A transient depression of blood lymphocyte (BL) responses to phytohemagglutinin (PHA), a T-cell mitogen, was observed over the first 8 weeks in the infected calves. Increases in BL responses to OAG were also observed. Differences were not observed in BL responses to pokeweed mitogen, a T- and B-cell mitogen. Blood lymphocyte responses to PHA in group-3 calves were low following the initial challenge exposure with OAG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse immune reactions and the pathogenesis of Ostertagia ostertagi infections in calves. 233 87


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