Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Structures of histamine-releasing peptides formed by the action of acid proteases on mammalian albumin(s). 247 9

Histamine release induced by compound 48/80 from rat mast cells is not dependent on extracellular Ca2+. Preincubation of mast cells with trypsin has only little effects on histamine release induced by this polycation. This work also demonstrates that histamine release induced by compound 48/80 and its analogues in the absence of extracellular Ca2+ depends on membrane bound sialic acid of the mast cell. Neuraminidase treatment of the cells in the presence of extracellular Ca2+ leads to histamine liberation. These findings suggest that sialic acid residues of the mast cell membrane constitute the site at which polycations exert their stimulatory actions of histamine liberation.
 ...
PMID:The role of membrane bound sialic acid of rat mast cells in histamine release induced by compound 48/80 and derivatives as well as calcium. 247 22

Glucocorticoids are potent anti-inflammatory drugs that are widely used in the treatment of allergic disorders. Their actions are often species specific or cell-type specific. Previous studies have demonstrated that glucocorticoids inhibit mediator release from mast cells derived from the peritoneum of mouse or rat and from guinea pig lung, but not those residing in human lung parenchymal tissue. In the present study, we have analyzed the effect of overnight culture with dexamethasone (10(-6) to 10(-7)M) on the subsequent IgE-dependent release of mediators from human mast cells derived from airway tissue, intestine, and skin. Airway tissue was passively sensitized with antigen-specific, IgE-rich serum during the culture period and subsequently challenged with ragweed antigen E. Skin and intestinal mast cells were challenged with anti-IgE. Histamine and immunoreactive LTC4 and PGD2 release was monitored in all experiments. Prostaglandin E release was quantitated in the experiments using airway tissue. Dexamethasone treatment failed to inhibit the release of mast cell mediators from all three tissues, but it inhibited the antigen-induced release of immunoreactive PGE from other cells residing in airway tissue. These results confirm earlier studies of the effects of glucocorticoids on human lung parenchymal mast cells, but contrast with the inhibitory effects of steroids observed in murine mast cells and human basophils.
 ...
PMID:Dexamethasone does not inhibit the release of mediators from human mast cells residing in airway, intestine, or skin. 247 59

The in vitro histamine release response of human intestinal mast cells and basophils challenged with anti-IgE, Concanavalin A, ionophore A23187 and food extracts was compared with skin prick test, RAST analysis and open food challenge. It was not possible to perform food challenge in all patients; however, seven children underwent open food challenge and in five the clinical diagnosis of "true" food allergy was confirmed. The intestinal mast cells were pooled from enzymatically dispersed duodenal biopsies obtained by duodenoscopy from 15 selected children suspected of food allergy, and five age-matched controls. In nine of 10 patients classified as "food allergic" intestinal mast cells released histamine to various food extracts in a dose-dependent fashion. From the mast cells of the nine food-allergic patients compared with non-allergics, the anti-IgE mediated mast cell histamine release was increased. Additionally, at 1000 U/ml anti-IgE the mast cell histamine release was increased compared with their corresponding basophils. However, in non-allergic subjects the histamine release of basophils was increased compared with their corresponding mast cells. Histamine release from basophils was positively correlated to the test scores of the RAST analysis, skin prick test, and food challenge. No apparent correlation between tests scores obtained from histamine release of intestinal mast cell and the other tests was demonstrated, except in children with diarrhoea as only symptom. However, the study gives evidence that duodenal mast cells actually are sensitized with specific IgE and thus may play a pathophysiological role in food hypersensitivity. In addition, the study shows that the ability of different stimuli, including food extracts, to trigger basophil histamine release does not correlate with their potency to induce histamine release from mast cells.
 ...
PMID:Comparison of intestinal mast cell and basophil histamine release in children with food allergic reactions. 248 85

The pathogenesis of burn edema in the skin of rats appears to be related to a role for histamine, xanthine oxidase and oxygen radicals. Histamine and its metabolic derivatives increase the catalytic activity of xanthine oxidase (but not xanthine dehydrogenase) in rat plasma and in rat pulmonary artery endothelial cells. In thermally injured rats levels of plasma histamine and xanthine oxidase rise in parallel, in association with increases in uric acid. Burn edema is greatly attenuated by treatment of rats with the mast cell stabilizer, cromolyn, by complement depletion and by treatment with the H2 receptor antagonist, cimetidine, but is unaffected by neutrophil depletion. These studies suggest the following pathogenesis of burn edema: thermal trauma causes complement activation with anaphylatoxin release and mast cell secretion of histamine, leading to enhancement of xanthine oxidase activity and increased production of oxygen radicals which damage endothelial cells.
 ...
PMID:Roles of histamine, complement and xanthine oxidase in thermal injury of skin. 257 May 31

Human leukocyte and skin mast cell preparations were incubated with morphine sulfate in concentrations ranging from 1.5 X 10(-5) M to 4.5 X 10(-3) M. Skin mast cells also were incubated with oxymorphone and fentanyl in the same concentrations. Human leukocytes did not release histamine in response to any concentration of morphine. In skin mast cells, histamine release by morphine first was detected at 1.5 X 10(-4) M. Histamine release further increased at 5.0 X 10(-4) M with no incremental increase at higher concentrations. Oxymorphone and fentanyl failed to release histamine at any concentration. Histamine release by morphine required calcium but was not influenced by changes in the 1-4 mM range. Skin mast cell preparations were pretreated for 30 min in naloxone 5 X 10(-4) M and then morphine 5 X 10(-4) M was added for 30 min without removing naloxone. Naloxone neither released histamine nor inhibited morphine-induced histamine release. The release of histamine by morphine but not equimolar concentrations of fentanyl and oxymorphone indicates that histamine release by narcotics is not a nonspecific effect of high drug concentration. The failure of naloxone to inhibit morphine-induced histamine release suggests that histamine release by morphine is not dependent on opiate receptor binding or activation. These results indicate that this human mast cell preparation will be useful in further understanding the mechanism of histamine release induced by morphine and other agents.
 ...
PMID:Comparison of histamine release in human skin mast cells induced by morphine, fentanyl, and oxymorphone. 257 52

The histology of 17 cases of basal cell carcinoma and dermis next to the carcinoma was observed. The results showed that the mast cell number was markedly increased in the dermis near the basal cell carcinoma. There was an increase in the collagen fibers between the carcinoma and dermis tissues, forming a thin membrane around the carcinoma tissue. These findings suggest that the carcinoma-associated antigen may activate the lymphocytes to produce certain lymphokine which stimulates the proliferation and differentiation of the mast cell precursors. Histamine and other active mediators released from mast cells stimulate fibroblasts to synthesize collagen fibers which form a thin membrane between the carcinoma and dermis. The membrane plays a protective role against tumor dissemination.
 ...
PMID:[Basal cell carcinoma and mast cells]. 263 34

Mast cells, endothelial cells, basophils and platelets are potential sources of histamine in the ovary. Little is known about the role of the latter three cell types in ovarian function. Several studies have revealed changes in the number and degranulation (release of histamine) of mast cells in the ovary during the cycle. Mast cells degranulate on pro-oestrus in the rodent ovary, and mast cells numbers increase in the theca externa of the dominant follicle in the bovine ovary. In rodents, mast cells are limited to the ovarian hilum and are not observed in follicles, corpora lutea and interstitium; this contrasts with larger species such as man, cows and monkeys where mast cells are observed throughout the ovary. Evidence is accumulating that mast cell degranulation in the ovary may be regulated by neuronal input. Neurones have been shown to have close morphological relationships with mast cells in the ovary. Histamine participates in regulating capillary permeability and blood flow in the ovary. These actions are induced by injections of LH, yet the mechanism by which LH induces mast cell degranulation is unknown. Histamine stimulates ovarian contractility, ovulation and follicular progesterone secretion in vitro. Whether these actions of histamine occur in vivo are currently unknown. This review gives a chronological description of the discoveries of the effects of histamine on ovarian function and makes suggestions for future research in this area.
 ...
PMID:Histamine, mast cells and ovarian function. 264 89

Tryptase from human mast cells is stabilized by negatively charged macromolecules such as heparin and is not affected by the protein inhibitors of serine proteinases normally present in human extracellular fluids. The current study demonstrated inhibition of tryptase-catalyzed cleavage of tosyl-Gly-Pro-Lys-p-nitroanilide by histamine and calcium, and destablization only by calcium. Calcium-mediated inhibition was competitive with a Ki of 30 mM. Cooperation of calcium with other extracellular cations or concentrations of calcium possible within cells or granules may permit calcium-mediated inhibition to occur in vivo. In contrast, only 5 mM calcium is needed to cause an irreversible 50% loss of tryptase activity after 60 min at room temperature. Histamine and N-methyl histamine concentrations of 2 mM to 10 mM inhibited tryptase activity by a different mechanism than calcium, resulting in sigmoid rather than hyperbolic kinetics. Whether this reflects cooperative binding of histamine to tryptase or conformational alterations of tryptase is not known. These concentrations of histamine are most relevant to those in mast cell secretory granules estimated at 100 mM, where tryptase is stored fully active and where histamine may play a role in attenuating tryptase activity.
 ...
PMID:Effect of histamine and divalent cations on the activity and stability of tryptase from human mast cells. 265 89

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.
 ...
PMID:Increased hyaluronan (hyaluronic acid) levels in bronchoalveolar lavage fluid after histamine inhalation. 272 57


<< Previous 1 2 3 4 5 6 7 8 9 10