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

We examined the temporal development and the fading in Sprague Dawley rats, actively sensitized to ovalbumin (OA), of the capacity of serosal mast cells, chopped lung tissue, and occasionally chopped tracheal tissue, to respond at antigen challenge in vitro with histamine release. Response capacity of both serosal mast cells and lung tissue developed within 2-3 weeks after injection of 1 microgram OA or more together with 100 mg of alum. Maximum response capacity was observed in cells and tissue from animals injected with 10 micrograms OA, part of the response capacity then remained until 3 months after immunization. Development of serosal mast cell reactivity was occasionally dissociated from that of lung tissue. When low amounts of alum (1 or 10 mg) were employed as adjuvant, lung tissue reactivity could be induced in the virtual absence of serosal mast cell response capacity. Silica gel was less efficient than alum as an adjuvant for induction of a primary response, but 'secondary' tissue responses could be induced when silica gel was used as an adjuvant. Pretreatment of the animals with cyclophosphamide before the booster injection enhanced and prolonged the response capacity of lung tissue. Animals injected with OA together with Freund's complete adjuvant did not provide responding serosal mast cells; response capacity of lung tissue varied with immunization dose of antigen. Antigen-induced histamine release from chopped tracheal tissue did not correlate to response capacity of lung tissue. Thus, the development in the rat of response capacity with respect to antigen-induced histamine release dissociates from serosal mast cells, lung tissue, and tracheal tissue.
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PMID:Antigen-induced release of histamine from rat tissues in vitro: dissociation in development of serosal mast cell, lung tissue, and tracheal tissue response capacity. 617

Anti-IgE- and Con A-induced histamine release from serosal mast cells were compared to each other and to total serum levels of IgE in non-immunized, alum-injected, and Silica gel-injected rats of the BN, Fischer, PVG, and SD strains. The results indicate that the degree of anti-IgE- and Con A-induced release is strain-dependent and varies with immunization conditions. Furthermore, there is a gross but not complete correlation between the degree of serosal mast cell histamine release induced by the two secretagogues. However, Con A- or anti-IgE-induced release could significantly be correlated to serum levels of total IgE only in the Fischer strain but not in the BN or the PVG strains. In the SD strain, Con A-induced release correlated to serum IgE levels in Silica gel-injected but not in alum-injected animals.
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PMID:Anti-IgE and Con A-induced histamine release from mast cells of four rat strains: correlation with total serum IgE. 618 92

PVG rats given injections of 1 microgram ovalbumin (OA) together with 10 mg Silica gel failed to provide serosal mast cells or lung tissue with the capacity to release histamine on in vitro challenge with the antigen. However, if such animals were injected i.p. with 100 mg of alum (without any further antigen addition) 3-9 weeks after the primary antigen injection, their mast cells and lung tissue showed a clear-cut capacity to respond in vitro, when examined 1 week after the alum injection. Injection of only 15 mg alum did not induce such a response capacity. The fading of the reactivity induced by an alum injection could be prevented by a repeated injection of the adjuvant alone. Pretreatment of the rats with cyclophosphamide (33 mg/kg) 2 days before the primary antigen injection did not affect the response capacity induced by a booster injection 3 weeks later. S.c. injection of alum also precipitated response capacity in animals primed by i.p. injection of antigen and Silica gel. The anaphylactic response capacity induced by injection(s) of alum was generally accompanied by increased levels of OA-IgE and especially OA-IgG2a antibody; however, a clear-cut correlation between either serosal mast cell or lung tissue response capacity and serum OA-IgE or IgG2a antibody titer could not be demonstrated. These data show that in primed animals, which do not express allergic response capacity, such a capacity can be induced by injecting adjuvant alone, even several weeks after the primary antigen injection.
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PMID:The non-specific enhancement of allergy. II. Precipitation of anaphylactic in vitro response capacity and serum IgE and IgG2a antibody synthesis in primed but non-responding rats by injection of alum. 619 90