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

The study describes the distribution of mast cells and of substance P (SP) and calcitonin gene-related peptide (CGRP)-immunoreactive nerve fibers in the rat palatal mucosa, focusing on the anatomic relationship between these tissue elements. The maxilla of 10-14-wk-old rats was dissected free, fixed, demineralized and frozen. Consecutive sections were stained with avidin peroxidase or processed for immunohistochemistry. In order to define the correlation between nerve fibers and mast cells, double staining techniques were used. The distance between each avidin-positive mast cell and the nearest detectable nerve fiber was determined. 5-Hydroxytryptamine- (5-HT) and avidin peroxidase-positive mast cells were frequently seen in the palatal mucosa but were rarely found in the gingival area. A large number of nerve fibers showing SP- and CGRP-like immunoreactivity were seen, particularly in association with blood vessels. Some nerve fibers were located in contact with or very close to the mast cells but the vast majority of mast cells showed no close anatomic association to nerve fibers. The nerve fibers and mast cells were mainly concentrated to the same regions in the palatal mucosa where blood vessels occurred. The observations suggest that in the rat palatal mucosa the main functional relationship relates to SP/CGRP and the blood vessels, and only to a minor degree to SP/CGRP and mast cells.
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PMID:Anatomic relationship between substance P- and CGRP-immunoreactive nerve fibers and mast cells in the palatal mucosa of the rat. 753 32

Clinical studies of vernal keratoconjunctivitis (VKC) patients show that total IgE serum levels are increased even in the absence of IgE antibodies to common allergens. Activated eosinophils are also a constant feature of VKC at both the circulation (cytofluorimetry) and tissue (tear cytology and conjunctival scrapings) levels. Moreover, allergen challenge induces a prolonged inflammatory reaction with a prevalent participation of eosinophils, lymphocytes and possibly basophils. Immunohistochemical studies of VKC biopsies show a multicellular inflammatory infiltrate with prevalence of activated eosinophils, mast cells and CD4 lymphocytes in both epithelium and subepithelium. Mediator studies indicate that eosinophil products (eosinophil peroxidase, eosinophinal cationic protein and eosinophil-derived neurotoxin/eosinophil protein X) are increased in both serum and tears, where tryptase and interleukin (IL)-5 are also detectable in higher amounts than in controls. On the basis of these findings, we postulate that VKC can represent a phenotypic model of up-regulation of the cytokine gene cluster on chromosome 5q which through its products (IL-3, IL-4, IL-5 and granulocyte/macrophage-colony-stimulating factor) regulates Th2 prevalence, IgE production as well as mast cell and eosinophil growth and function in VKC.
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PMID:Vernal keratoconjunctivitis: a model of 5q cytokine gene cluster disease. 761 25

Mast cells are important effector cells in IgE-mediated acute allergic reactions. Mast cells also produce cytokines such as interleukin (IL)-3, IL-4, IL-5, tumor necrosis factor (TNF), and granulocyte-macrophage colony-stimulating factor (GM-CSF) that regulate the function of eosinophils and the development of a late-phase inflammatory response to antigen challenge. To evaluate the role of mast cells on the development of IgE-mediated allergic pulmonary eosinophilia in vivo, we compared the eosinophil infiltration into lungs of mast cell deficient mice (WBB6F1/J-W/Wv) with their congenic normal littermates (W/W+). Mice were sensitized with alum-precipitated ovalbumin and challenged with aerosolized ovalbumin on day 12 after sensitization. Bronchoalveolar lavage (BAL) fluid, lung tissue biopsies, and blood samples were collected after ovalbumin challenge. Eosinophil numbers in the BAL and lung tissue, lung eosinophil peroxidase (EPO) activity and serum levels of IgE and IgG1 were measured. In sensitized W/W+ mice, there were increased numbers of eosinophils in the BAL fluid and lung tissue, and EPO levels were increased after ovalbumin challenge. Ovalbumin challenge of sensitized mast-cell-deficient mice produced fewer numbers of eosinophils in the BAL fluid and lungs, and EPO levels were also reduced compared with their challenged congenic littermates. On the other hand, levels of serum IgE and IgG1 were not different between W/Wv mice and their congenic littermates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mast cells modulate allergic pulmonary eosinophilia in mice. 769 19

The growing recognition of asthma as an immunologic disease mediated by inflammatory cells and mediators has changed the nature of therapy and monitoring of this disease. Modulation of inflammatory mediators such as leukotrienes, prostaglandins, and adenosine by specific immunoregulatory pharmacotherapy is now becoming well-recognized as essential for proper management of allergic diseases, including asthma. The newly-developed immunoassays for specific inflammatory cell activation markers, such as tryptase for mast cell activation, myeloperoxidase for neutrophil activation, and eosinophilic cationic protein (ECP) and eosinophil-derived neurotoxin (EDN) for eosinophil activation, may significantly enhance the ability to both determine the cellular etiology of allergic inflammation and also to monitor the efficacy of antiinflammatory therapies in suppressing cell-specific immunologic events.
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PMID:Introduction: mediator assays and inflammatory events in asthma and allergic disease (Immunology Research Institute of New England Symposium). 792 8

Several lines of evidence document a critical role for mast cells in immune complex-mediated inflammatory models. However, their role in nonimmune models of acute inflammation is largely unknown. In the present investigation, the role of mast cells was examined in calcium ionophore (A23187)-induced mouse peritoneal inflammation. Intraperitoneal injection of A23187 (20) micrograms/mouse) elicited marked and transient increases in immunoreactive levels of 6-ketoprostaglandin-F2 alpha, leukotrienes B4, C4, D4, E4, and F4. There were no discernible differences in levels of these mediators in male Swiss Webster mice, mast cell-deficient mice (WBB6F1-W/W'), and age-matched controls (WBB6F1-+/+), suggesting a minimal role of mast cells in eicosanoid biosynthesis in this model. However W/W' mice showed smaller increases in levels of myeloperoxidase, a marker for neutrophils, compared to +/+ mice. Both W/W' and +/+ mice have lower constitutive levels of peritoneal N-acetyl-beta-D-glucosaminidase (NAG), a marker for mononuclear cells. Similar to the changes seen in myeloperoxidase, W/W' mice exhibited a blunted NAG response compared to +/+ mice. These results suggest that mast cell products other than eicosanoids may contribute to the changes in cellular trafficking in response to intraperitoneal A23187. These results also suggest that mast cells are required for full expression of inflammatory responses.
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PMID:Role of mast cells in calcium ionophore (A23187)-induced peritoneal inflammation in mice. 807 Sep 2

The objective of this study was to determine whether ischemia-reperfusion (I/R) of the small bowel activated mast cells and, if so, to determine whether this event contributed to granulocyte infiltration and mucosal barrier dysfunction. Autoperfused segments of the jejunum were exposed to 30 min of ischemia followed by 60 min of reperfusion. Epithelial permeability was assessed by the clearance of 51Cr-labeled EDTA from plasma to lumen. Plasma rat mast cell protease II (RMCP II) was measured and used as an index of mucosal mast cell degranulation, whereas myeloperoxidase (MPO) activity was used as an index of granulocyte infiltration. I/R caused a significant increase in plasma RMCP II levels, MPO activity, and epithelial permeability. The mucosal mast cell stabilizer doxantrazole prevented the I/R-induced increase in all three parameters. The connective tissue mast cell stabilizer ketotifen had no effect. To determine whether oxidants were involved in mast cell degranulation, some animals were pretreated with superoxide dismutase and catalase. This regimen completely abolished the I/R-induced rise in plasma RMCP II levels and attenuated mucosal MPO activity and epithelial permeability. Selective inhibitors of two mast cell-derived mediators, platelet-activating factor and histamine, did not attenuate the rise in epithelial permeability. These data suggest that oxidant-induced mucosal mast cell degranulation is a key event in the granulocyte infiltration and tissue dysfunction associated with reperfusion of the ischemic intestine.
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PMID:Mast cells contribute to ischemia-reperfusion-induced granulocyte infiltration and intestinal dysfunction. 807 30

The effects of topical application of arachidonic acid (AA) or phorbol ester, tetradecanoylphorbol 13-acetate (TPA), on edema response, vascular permeability, MPO, NAG, and generation of eicosanoids were studied in two murine models of cutaneous inflammation. AA produced a short-lived edema response with a rapid onset that was associated with marked increases in levels of prostaglandins (PGE2, 6-keto-PGF1 alpha, PGF2 alpha), thromboxane B2 (TxB2) and leukotriene B4 (LTB4), with smaller increases in levels of LTC4. TPA produced a longer-lasting edema that was associated with marked influx of neutrophils and predominant formation of LTB4 along with significant changes in levels of TxB2. Circulating T lymphocytes have no apparent role in the acute inflammatory responses induced by either agent. Arachidonic acid-induced vascular permeability preceded the edema response and neutrophil influx, whereas TPA-induced vascular permeability paralleled the edema response and influx of neutrophils. Mast cells appear to be important in the complete expression of inflammatory response, i.e., edema, cellular influx, and vascular permeability induced by either AA or TPA, as these responses were blunted in mast cell-deficient mice. Inhibitors of CO or 5-LO attenuated inflammatory responses in both models. The LTB4 receptor antagonist, SC-41930, inhibited the inflammatory response to TPA but had little effect on that initiated by AA. This suggests that LTB4 is an important mediator in the phorbol ester-induced inflammatory response, whereas peptidoleukotrienes and prostaglandins regulate vascular permeability responses in the arachidonate model.
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PMID:Comparative evaluation of arachidonic acid (AA)- and tetradecanoylphorbol acetate (TPA)-induced dermal inflammation. 811 31

Mast cell hyperplasia and changes in phenotypic characteristics subsequent to myenteric and extrinsic denervation of a segment of rat jejunum were studied. The myenteric plexus and extrinsic nerves were ablated by serosal application of the cationic surfactant benzyldimethyltetradecylammonium chloride. There was a four-fold increase in the number of mast cells in the smooth muscle layers 15 days after denervation. This increase was sustained for at least 90 days after treatment. No increase in mast cell number was observed in the villus-crypt axis of the jejunum. Berberine sulfate fluorescent detection of heparin-containing mast cells demonstrated that a change in mast cell phenotype occurred between 20 and 90 days after the denervation procedure. The fact that myeloperoxidase activity was the same in denervated and control tissue within 5 days of denervation demonstrates the lack of a chronic inflammatory reaction. Our results suggest that mast cells might play a role in the gut wall re-modeling processes.
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PMID:Proliferation of mast cells in the smooth muscle of denervated rat jejunum. 828 47

We studied the distribution of histamine (HA) immunoreactivity in endocrine cells of the acid-producing mucosa in rat stomach with pre-embedding immunoelectron microscopy (IEM) using an antiserum against HA. Four fixation modifications were compared to optimize the ultrastructural morphology and staining pattern with the antisera produced against carbodiimide-conjugated HA. Fixation with 4% 1-ethyl-3(3-dimethyl-aminopropyl) carbodiimide (EDCDI) combined with both 4% paraformaldehyde and 0.1% glutaraldehyde gave superior results compared with EDCDI alone. Enterochromaffin-like (ECL) cells were easily distinguished from other endocrine cells in optimally fixed samples. The peroxidase end-product was distributed within the cytoplasm surrounding the vesicles of the ECL cells. ECL cells comprised about 75% of all endocrine cells, and about 90% of them were HA immunoreactive (HA-IR). No other HA-IR cell types were identified by EM in the basal half of the oxyntic region of rat gastric mucosa. The results suggest that a combination of EDCDI and aldehydes is suitable for IM demonstration of HA in cells. ECL cells from a predominant portion of endocrine cells in the oxyntic glands and may constitute the only significant non-mast cell store of HA in rat gastric mucosa.
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PMID:Histamine-storing cells in the oxyntic mucosa of the rat stomach: a transmission electron microscopic study employing fixation with carbodiimide. 835 80

Anti-inflammatory properties have been ascribed to a series of N-(fluorenyl-9-methoxycarbonyl) amino acids called leumedins that inhibit the activity of granulocytes and T-lymphocytes. We evaluated one of these leumedins, N-(fluorenyl-9-methoxycarbonyl) leucine (NPC 15199), in a model of ileitis in guinea pigs. Ileitis was induced by intraluminal trinitrobenzenesulfonic acid (TNBS 30 mg/kg in 50% ethanol) in anesthetized guinea pigs. NPC 15199 was administered daily (10 or 100 mg/kg, s.c.). After 7 days, the guinea pigs were anesthetized, and saline was administered intraluminally into an ileal loop created at the site of TNBS administration and was withdrawn after 30 min. The changes in lavage protein, nitrite levels, myeloperoxidase (MPO) activity and mast cell numbers were used as indices of inflammation and injury. NPC 15199 (10 or 100 mg/kg) attenuated or abolished TNBS-induced elevations in lavage protein and nitrite content. Only the high dose of NPC 15199 (100 mg/kg) attenuated ileal MPO activity and mast cell hyperplasia. Histological disturbances induced by TNBS administration included crypt hypertrophy, mucosal and submucosal fibrosis and smooth-muscle hyperplasia. These disturbances were reversed by high-dose NPC 15199 (100 mg/kg) but were minimally affected by low-dose NPC 15199 (10 mg/kg). We conclude that NPC 15199 prevents mucosal injury and dysfunction in this model of intestinal inflammation. Inhibition of granulocyte infiltration does not appear to be essential for the beneficial effects of NPC 15199 and suggests that the alternative actions of NPC 15199 may be pertinent to this model.
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PMID:Guinea pig ileitis is attenuated by the leumedin N-(fluorenyl-9- methoxycarbonyl)-leucine (NPC 15199). 839 62


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