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 effect of dialysable thymic extract on the IgE-antibody production in rats was studied. A marked suppression of IgE-antibody production determined by mast cell degranulation and passive cutaneous anaphylaxis tests was found in the immunized rats injected with dialysable thymic extract. The treatment of this preparation with immobilized pronase affects neither its suppressive activity, nor does such treatment affect the activity of purified factor, isolated from the crude extract. The prolonged administration of purified preparation to rats leads to an increase in thymus weight. When syngeneic thymocytes incubated with purified non-polypeptide thymic factor were administered to immunized rats a significant suppression of IgE-antibody production was observed compared to that occurring in untreated ones. On this basis, it was concluded that a decrease of IgE-antibody production may be due to a direct stimulation of T-suppressor cells.
 ...
PMID:Suppression of IgE-antibody production by non-polypeptide dialysable thymic factor. 31 57

To investigate mechanisms of mast-cell proliferation, we have utilized infection of Lewis rats with the intestinal nematode, Nippostrongylus brasiliensis, which induces a pronounced intestinal mast-cell hyperplasia. Adoptive transfer of 2 x 10(8) immune mesenteric lymph node cells (IMLN), collected 14 days post infection with 3000 third stage larvae (L3), into rats concurrently given 3000 L3 hastened the expected intestinal mastocytosis by up to 4-5 days. IMLN exhibited this mastopoietic activity in the presence but not in the absence of concurrent infection. Normal mesenteric lymph node cells did not show similar mastopoietic activity. Intestinal mastocytosis was delayed by sub-lethal irradiation (400 rad) but IMLN reconstituted the mast-cell response of such animals. The mastopoietic activity could not be attributed to worm antigen as antigen administered intravenously had no significant effect on mastocytosis and furthermore, antigen could not be detected in mastopoietically active IMLN suspensions used as a possible antigen source in passive cutaneous anaphylaxis tests. Immune serum (14 days post primary infection with 3000 L3) also hastened mastocytosis in infected rats, whereas normal serum did not. The IMLN may be an enriched source of intestinal mast cell precursors and, in addition, may contain a cell type(s) which regulates the differentiation and proliferation of such precursors.
 ...
PMID:Immunologically mediated intestinal mastocytosis in Nippostrongylus brasiliensis-infected rats. 31 19

The role of the mouse homocytotropic antibodies in passive cutaneous anaphylaxis reaction was investigated. One class of antibody was heat stable, detected at 2 h but not at 48 h after passive transfer, and belonged to a sublcass of mouse IgG. The other was heat labile, detected at 2 h and 48 h after passive transfer, and belonged to the IgE class of mouse immunoglobulins. In the presence of IgG, IgE homocytotropic antibody was not detected early after passive transfer. This was thought to be due to a masking of IgE by IgG antibodies rather than a competition for mast cell surface receptors, since inhibition studies with rat IgE myeloma protein suggested that mouse IgE and IgG1 may have different receptor sites on mast cell surfaces.
 ...
PMID:Role of mouse IgG and IgE homocytotropic antibodies in passive cutaneous anaphylaxis. 34

Five patients with asthma and severe aspirin hypersensitivity were challenged on separate days with increasing doses of aspirin given by mouth, starting with 5 mg, until a reduction in FEV1 greater than 15% was obtained. Sodium cromoglycate in doses of 20-40 mg inhibited the bronchoconstrictive reaction not only when inhaled before the challenge but also after it, at a time when progressive reduction in FEV1 values was taking place. According to these results, it seems reasonable to postulate sequential mast cell degranulation and liberation of mediators of anaphylaxis as the mechanism through which aspirin induces bronchoconstriction in aspirin-sensitive asthmatics. The differences between bronchial provocation tests and oral challenge with aspirin are stressed.
 ...
PMID:Inhibition of aspirin-induced bronchoconstriction by sodium cromoglycate inhalation. 41 71

The topographic distribution, population density, and ultrastructural features of metachromatic cells (mast cells and basophilic leukocytes) were studied in lung biopsies from five control patients and 17 patients with fibrotic lung disorders. The great majority of metachromatic cells were mast cells. The average number of metachromatic cells per square millimeter of tissue section was much larger in patients with fibrotic lung disorders (45.8 +/- 6.5) than in control patients (2.6 +/- 1.6). In control patients, mast cells were most frequently seen in subpleural and perivascular connective tissue. In contrast, the vast majority of mast cells in patients with fibrotic lung disorders was present in thickened, fibrous alveolar septa; mast cells also were found within the alveolar epithelial layer and alveolar lumina. The quantitative distribution of different types of mast cell granules differed in the two groups of patients: granules composed of scrolls were more frequent in control patients, and granules of the combined type (containing mixtures of different components within the same granule) were more frequent in patients with fibrotic lung disorders. Mast cells in the latter patients appeared to migrate through defects in the basement membrane into the epithelial layer and alveolar lumina; mast cells in these areas often showed reduced numbers of granules and disorganized granule content. These changes suggest that pulmonary parenchymal mast cells in fibrotic lung disorders undergo a chronic process of partial degranulation which differs from that found in anaphylaxis; this chronic release of mast cell products may contribute to the continuing alveolar injury and the ventilation-perfusion inequalities observed in the fibrotic lung disorders.
 ...
PMID:Ultrastructure of pulmonary mast cells in patients with fibrotic lung disorders. 44 78

A peptide of approximately 300-400 daltons exhibiting in vitro chemotactic activity for human polymorphonuclear (PMN) leukocytes, with a preference for the eosinophil series, was isolated from extracts of anaplastic lung carcinomas of the large squamous cell type obtained from three patients with marked peripheral blood hypereosinophilia and eosinophilic infiltration of the tumors and surrounding normal pulmonary tissues. This chemotactic factor was termed ECF-LSC (eosinophil chemotactic factor of lung squamous cell carcinoma). ECF-LSC appeared in the urine of two of the patients in increasing quantities late in the course of their disease and was also elaborated by long-term cultures of dispersed tumor cells from the same two patients. Three anaplastic large cell bronchogenic carcinomas which were not associated with tumor tissue or peripheral blood eosinophilia, a bronchogenic adenocarcinoma from a patient with only peripheral eosinophilia, and a renal cell carcinoma metastatic to the lungs and associated with transient pleural tissue and fluid eosinophilia were all devoid of ECF-LSC. ECF-LSC from tumor tissue extracts, urine, and tumor cell culture medium was comparable to the mast cell-associated tetrapeptides of the eosinophil chemotactic factor of anaphylaxis (ECF-A) in size, but eluted from Dowex-1 at pH 5.0-3.5 in contrast to the more acidic ECF-A tetrapeptides which eluted at pH 3.2-2.2 ECF-LSC, like the tetrapeptides of ECF-A, had a secondary chemotactic activity for neutrophil PMN leukocytes, but not mononuclear leukocytes, and deactivated both eosinophil and neutrophil PMN leukocytes so that they would not respond to a subsequent in vitro chemotactic stimulus. Eosinophils from the two patients with urinary excretion of ECF-LSC and the highest concentrations in tumor extracts were hyporesponsive in vitro to homologous and heterologous chemotactic stimuli, suggesting that ECF-LSC had deactivated the eosinophils in vivo.
 ...
PMID:Production of a low molecular weight eosinophil polymorphonuclear leukocyte chemotactic factor by anaplastic squamous cell carcinomas of human lung. 64 Nov 54

Studies were performed in animals to establish whether antigen prefeeding could present homocytotropic antibody synthesis and the induction of gastric ulcer resulting from mucosal anaphylaxis. A single digestive exposure to 1 or 10 mg ovalbumin induced a state of specific immunologic tolerance. Inhibition of the formation of specific reagins was shown by the study of mast cell degranulation. Tolerant animals presented a reduced incidence of gastric ulcer after subsequent mucosal challenge. These results are important for the development of methods of prevention and treatment of allergic diseases.
 ...
PMID:Prevention of experimental anaphylactic ulcer by antigen prefeeding. 75 29

Eosinophil migration toward a concentration gradient of a chemotactic factor is regulated at four levels. Diverse immunologic pathways generate stimuli with eosinophil chemotactic activity, including the complement products C5a and a fragment of C3a and the peptide products of mast cells and basophils activated by IgE-mediated reactions, such as eosinophil chemotactic factor of anaphylaxis (ECF-A) and other oligopeptides. The intrinsic preferential leukocyte activity of the chemotactic stimuli represents the second level of modulation, with ECF-A and other mast cell-derived peptides exhibiting the most selective action on eosinophils. The third level of control of eosinophil chemotaxis is composed of inactivators and inhibitors of chemotactic stimuli and is exemplified by degradation of C5a by anaphylatoxin inactivator or chemotactic factor inactivator and of ECF-A by carboxypeptidase-A or aminopeptidases. The activity of ECF-A is uniquely suppressed by equimolar quantities of its NH2- terminal tripeptide substituent, presumably by eosinophil membrane receptor competition. Factors comprising the fourth level of regulation, which alter eosinophil responsiveness to chemotactic stimuli, include the chemotactic factors themselves, through deactivation; nonchemotactic inhibitors such as the COOH-terminal tripeptide substituent of ECF-A, the neutrophil-immobilizing factor (NIF), the phagocytosis-enhancing factor Thr-Lys-Pro-Arg, and histamine at concentrations greater than 400 ng/ml; and nonchemotactic enhancing principles represented by ascorbate and by histamine at concentrations of 30 ng/ml or less. Local concentrations of eosinophils called to and immobilized at the site of a hypersenitivity reaction may express their regulatory functions by degrading the chemical mediators elaborated including histamine, slow-reacting substance of anaphylaxis (SRS-A), and platelet-activating factor (PAF) by way of their content of histaminase, arylsulfatase B, and phospholipase D, respectively. Immunologic pathways may thus provide the capability for early and specific host defense reactions with a later influx of eosinophils preventing irreversible local tissue alterations or distant organ effects.
 ...
PMID:Modulation of human eosinophil polymorphonuclear leukocyte migration and function. 79 10

Allergic asthma is caused by antigen reaction with IgE fixed to mast cells of the bronchi. The reaction causes release of slow-reacting substance of anaphylaxis and histamine, which cause bronchial constriction. Prophylactic treatment includes avoidance of antigens, desensitization and use of cromolyn sodium. The latter appears to impede release of chemical mediators by the mast cell. Although of no value during an acute attack, this agent reduces attacks and reduces the need for other drugs in patients with severe perennial asthma.
 ...
PMID:Approaches to asthma management. 80 65

Infection of CFW mice with Trichinella spiralis induced a state of relative unresponsiveness to passive cutaneous anaphylaxis (PCA) induced with hen egg albumin and its corresponding antibodies. The unresponsiveness was to PCA produced either with immunoglobulin G1 (IgG1) or IgE type of antibodies, but was more pronounced with the latter. As few as 25 larvae given by stomach tube 20 days before induced this resistance, although 400 larvae induced a greater resistance. When 400 to 600 larvae were fed to mice, the refractoriness of these mice to PCA was noticed 15 days later. The sera of infected mice had the ability to inhibit mainly PCA induced by IgE. This inhibitory property of sera from infected mice was more pronounced 35 days after infection than 10 months later, when only weak inhibitory activity was detected. Purified rat IgE inhibited the PCA reactions induced in both mice and rats with mouse IgE-type antibody. At high concentrations, evidence of inhibition of the IgG1-induced PCA in mice was also obtained. We believe that the relative unresponsiveness of infected mice is due to an increase in production of IgE which competitively blocks the mast cell sites for other IgE molecules.
 ...
PMID:Effect of Trichinella spiralis infection on passive cutaneous anaphylaxis in mice. 83 10


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