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

Electrical stimulation (ES) of sensory nerves causes increased vascular permeability and vasodilatation, a process known as neurogenic inflammation. The purpose of this study was to assess the role of mast cells in neurogenic inflammation induced by ES of sensory nerves. ES of the rat saphenous nerve for 1, 3, 5, 15, or 30 min induced a 166 to 436% increase in the amount of 125I-albumin deposited in the skin. Through the initial 15 min of ES, the histamine content of the skin remained unchanged. However, 30 min of ES caused a 22.1% decrease in skin histamine (p less than 0.05). ES for 5 min followed by measurement of vascular permeability from 0 to 30 min thereafter resulted in maximal increases in 125I-albumin in the skin immediately after cessation of the pulse of ES. When skin histamine was measured at various intervals after a 5-min pulse of ES, no change in the histamine content was observed through the subsequent 30 min. When mast cell degranulation was assessed histologically, 5 min of ES failed to stimulate mast cell degranulation. However, 30 min of ES caused a significant increase in the proportion of degranulating mast cells. When draining venous plasma histamine was monitored before, during and after ES, no change in plasma histamine was observed. In contrast, the intradermal injection of 5 micrograms of compound 48/80 produced a significant increase in plasma histamine. In order to examine the possibility that histamine might be released but remain in the skin after ES, skin "blisters" were developed by intradermal injections of saline. There was a significant increase in the amount of 125I-albumin extravasated into blister fluid measured after 3, 5, and 10 min of ES and a significant increase in histamine after 5 or 10 min. Therefore, prolonged ES of sensory nerves can cause mast cell degranulation. However, ES causes increased vascular permeability at times when no mast cell activation can be observed. These data suggest that the initial phases of neurogenic inflammation are independent of mast cell activation.
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PMID:Neurogenic inflammation, vascular permeability, and mast cells. 245 60

We have developed a model of IgE-dependent, mast cell-mediated arthritis in rats. One knee joint (test joint) of a Sprague-Dawley rat was injected with 1 micrograms of a monoclonal IgE specific for dinitrophenol, and the contralateral (control) joint was injected with the same amount of an irrelevant monoclonal IgE in phosphate buffered saline or with phosphate buffered saline alone. Within 5 minutes of intravenous injection of antigen, an acute, transient arthritis occurred in the test joints only, with swelling and extravasation of intravascular blue dye and 125I-labeled albumin, decreased numbers of stainable mast cells, and decreased histamine content of the joint synovium. Pretreatment of experimental animals with H1 and H2 antihistamines did not completely block the reaction. These data show that IgE-dependent synovial mast cell degranulation causes a transient, nondestructive arthritis, reminiscent of lupus arthritis and intermittent hydrarthrosis.
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PMID:Demonstration and characterization of a transient arthritis in rats following sensitization of synovial mast cells with antigen-specific IgE and parenteral challenge with specific antigen. 245 75

1. Medium conditioned by rat neutrophils stimulated by N-formyl-methionyl-leucyl-phenylalanine (FMLP) has been found to generate mast cell histamine-releasing activity (HRA) when incubated with bovine serum albumin (BSA). 2. Histamine release increased as the concentration of BSA used to generate HRA was increased from 0.25 to 10 mg ml-1, as the concentration of neurotrophil conditioned medium was increased and as the concentration of FMLP used to stimulate the neutrophils was increased. Histamine release was non-cytotoxic as it was inhibited by energy deprivation or by removal of calcium and it was accompanied by degranulation. 3. HRA was detectable after 30 min of incubation with BSA and its generation continued to increase over the 18 h of our measurements. 4. Generation of HRA was dependent upon the presence of medium from stimulated neutrophils and on the presence of BSA, although plasma could substitute for BSA. Likewise, HRA could be generated from gamma-globulin although to a lesser extent than with albumin. 5. Generation was optimum at acid pH and was inhibited by prior boiling of the neutrophil conditioned medium or by the addition of pepstatin. 6. It is suggested that an enzyme(s) released from the neutrophil during stimulation acts on an albumin-like substrate to generate HRA. It is proposed that HRA is peptide in nature and may be generated during an inflammatory response.
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PMID:Generation of histamine-releasing activity from serum albumin by medium derived from stimulated neutrophils of rat. 247 47

The acid proteases, pepsin, rennin and cathepsin D, were shown to generate mast cell histamine releasing peptides (HRP) when incubated with the albumin fraction of mammalian plasmas. Significant histamine release was observed using less than 1 microliter equivalent of pepsin-treated plasma. Histamine release was rapid, dependent on calcium and energy, and accompanied by degranulation. The major HRP present in pepsin-treated human and canine plasma was identified as H-Ile-Ala-Arg-Arg-His-Pro-Tyr-Phe-OH whereas that from rat plasma had valine substituted for isoleucine. Cathepsin D-treated BSA gave rise to the human octapeptide (above) as well as to an extended decapeptide with H-Tyr-Glu- at the N-terminus. These peptides were apparently derived from one region of serum albumin, residues 139 to 149 of the human, canine, or bovine sequence. We hypothesize that cathepsin D, released from leukocyte lysosomes, might generate HRP during the delayed phase of an inflammatory response.
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PMID:Structures of histamine-releasing peptides formed by the action of acid proteases on mammalian albumin(s). 247 9

Antigen challenge of jejunal epithelium from rats sensitized to egg albumin induces an active Cl- secretory process secondary to release of mucosal mast cell mediators. The present study was designed to define the relative role of these mast cell mediators and the enteric nervous system in the transport abnormalities associated with intestinal anaphylaxis. Net ion transport of stripped jejunal tissue from sensitized and sham-treated animals was studied in Ussing chambers. The Cl- secretory response induced by egg albumin during intestinal anaphylaxis was similar to that after addition of 5-hydroxytryptamine (5-HT), histamine, and prostaglandins D2 and E2 to jejunal tissue. Cinanserin, a 5-HT2-receptor antagonist, virtually abolished the response to 5-HT and totally abolished the response to egg albumin. Methysergide, a 5-HT1-receptor antagonist had no effect on either response. Indomethacin, an inhibitor of prostaglandin synthesis, significantly inhibited the 5-HT and egg albumin response. Diphenhydramine, an H1-receptor antagonist and cimetidine, an H2-receptor antagonist both significantly inhibited the histamine response but neither altered the response to egg albumin. Atropine, an anticholinergic, and tetrodotoxin, a nerve blocker, did not inhibit the antigen induced anaphylactic response. These results indicate that 5-HT, acting through 5-HT2 receptors is largely responsible for the transport abnormalities seen in intestinal anaphylaxis induced by egg albumin while prostaglandins appear to play a partial role. The findings do not support a role for the enteric nervous system for the egg albumin induced changes in Cl- secretion.
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PMID:Intestinal anaphylaxis in the rat: mediators responsible for the ion transport abnormalities. 251 72

A double blind, placebo-controlled, cross-over study was performed to determine the effect of cetirizine, an H1 antihistamine, on the immediate nasal allergic response. Ten persons underwent nasal challenge with antigen after premedication with 20 mg of cetirizine or placebo QD for 2 days. The response was monitored by counting the number of sneezes and by measuring the levels of histamine, prostaglandin D2, leukotriene C4, albumin, and TAME-esterase activity in recovered nasal lavages. The results showed a significant reduction in sneezing and in the amounts of recovered albumin, TAME-esterase activity, and leukotriene C4 but no reduction in the amounts of recovered histamine and prostaglandin D2. These results suggest that cetirizine does not inhibit mast cell activation but inhibits the consequences of the released histamine on H1 receptors: sneezing and increased vascular permeability. The results further suggest that mast cell release of histamine is the direct result of antigen stimulation, as opposed to reflex activation, and that other cells in addition to mast cells generate leukotrienes during the early allergic response.
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PMID:The effect of cetirizine on early allergic response. 256 79

To increase understanding of the effect of H1 antihistamines on the immediate response to nasal challenge with antigen, we performed two double blind, placebo-controlled, crossover studies using cetirizine and terfenadine. The subjects underwent nasal challenge with antigen after premedication with either cetirizine (20 mg QD for two days, n = 10), terfenadine (60 mg BID for 1 week, n = 12), or placebo for equivalent periods of time. We monitored the response to challenge by counting the number of sneezes and by measuring the levels of inflammatory substances in recovered nasal lavages. Compared with placebo, both antihistamines significantly reduced sneezing and the levels of recovered albumin and TAME esterase activity, suggesting that both reduced the expected increase in vascular permeability. With cetirizine, there was also a reduction in the levels of LTC4 (not measured in terfenadine studies) but not in those of recovered histamine and prostaglandin D2. These data suggest that cetirizine did not affect mast cell mediator release, that histamine release is due to the direct action of antigen stimulation and that leukotrienes are generated by cells in addition to mast cells. With terfenadine, there were significant reductions in the levels of histamine and kinins (not measured in cetirizine study) seen after nasal challenge with antigen. The reduction in kinins most likely reflects alteration in vascular permeability, whereas the effect on histamine presumably reflects inhibition of mast cell activation. When combined, these experiments demonstrate effects of H1 antihistamines on histamine release beyond those usually described, as well as differences between drugs within a single classification.
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PMID:The effects of H1 antihistamines on the early allergic response. 257 50

The effect of immunoglobulin E (IgE)-mediated anaphylaxis has been extensively studied in the small intestine, but little information is available on the response of the stomach to IgE-mediated mucosal reactions to food proteins. The effect of luminal antigenic challenge on gastric acid secretion, gastric emptying, and mucosal mast cell degranulation was examined in rats sensitized to egg albumin or in sham-treated controls. Intraluminal challenge of the stomach with egg albumin in sensitized animals significantly increased gastric acid secretion and delayed gastric emptying. The response was specific for the sensitizing antigen as challenge with bovine serum albumin was without effect. Sham-treated animals showed no response to egg albumin or bovine serum albumin. The increase in gastric acid secretion was reproduced by antigen challenge in naive animals passively transferred with hyperimmune serum. This effect was abolished by prior heat treatment of the serum. In sensitized animals challenged with egg albumin, there was histological evidence of mast cell degranulation in the stomach mucosa, increased intraluminal release of histamine, and increased serum levels of rat mast cell protease II, a marker specific for mucosal mast cell degranulation. The findings indicate that the stomach is a target organ for IgE-mediated reactions to food proteins. Antigen challenge in sensitized animals leads to increased gastric acid secretion and delayed emptying and evidence of mucosal mast cell activation.
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PMID:Gastric response to mucosal IgE-mediated reactions. 259 6

Hyaluronan (hyaluronic acid) appears in low concentrations in bronchoalveolar lavage fluid from healthy individuals, while increased amounts have been reported in lavage fluid from patients with interstitial lung diseases and allergic asthma. We have earlier reported a strong correlation between the appearance of lavage fluid mast cells and hyaluronan in patients with sarcoidosis and extrinsic allergic alveolitis. The central role of the mast cell in allergic asthma is well documented. In this study we have investigated if challenge with inhaled histamine, a major mast cell component, could influence the appearance of hyaluronan in bronchoalveolar lavage fluid. A more than twofold increase of hyaluronan was seen 24 h after challenge with histamine. This increase correlated with a less pronounced increase of albumin in lavage fluid. Histamine challenge also induced an increase of mast cells, lymphocytes, and granulocytes in the lavage fluid. The observed histamine effect on the hyaluronan recovery during lavage might be explained by a histamine-mediated leakage of interstitial fluid, rich in hyaluronan, to the alveolar space. Mast cell degranulation of histamine may partly underlie the appearance of increased amounts of hyaluronan in lavage fluid from patients with interstitial lung diseases and allergic asthma.
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PMID:Increased hyaluronan (hyaluronic acid) levels in bronchoalveolar lavage fluid after histamine inhalation. 272 57

Our previous studies demonstrated that rats sensitized to egg albumin had reduced intestinal absorption of water and electrolytes in response to intraluminal antigen. The rapid onset of this effect and reduction in mucosal histamine and numbers of granulated mast cells in the lamina propria suggested a reaginic (IgE) mechanism involving mast cell mediators. In this study we examined the effect of antiallergic agents on the intestinal transport abnormalities in our model. Sensitized rats, 14 days after intraperitoneal injection of 10 micrograms of egg albumin plus alum had specific IgE serum titers greater than or equal to 1:64; control rats had no measurable IgE antibodies. Net fluxes of Na+, Cl-, and H2O were determined by in vivo perfusion during a 1-hour antigen-free period and then a 1-hour antigen period. Sodium cromoglycate, administered intravenously (20 mg/kg) or in the perfusate (5 X 10(-4) mol/L) failed to prevent mucosal mast cell degranulation as evidenced by histamine release or the decrease in absorption of H2O, Na+, and Cl- induced by antigen exposure. In contrast, 10(-3) mol/L of doxantrazole in the perfusate completely inhibited these changes. Histamine receptor antagonists, H1, diphenhydramine, or H2, cimetidine, in perfusates had no effect on the transport abnormalities. Our findings support a role for intestinal mucosal mast cells, but not connective tissue mast cells, in the pathogenesis of the intestinal dysfunction associated with mucosal IgE-mediated reactions to food proteins and suggest that mast cell mediators other than histamine are involved.
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PMID:Transport abnormalities during intestinal anaphylaxis in the rat: effect of antiallergic agents. 286 97


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