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)

The findings reported here demonstrate that PGE2 can exert both anti- and pro-inflammatory activities in one and the same tissue, as exemplified by inhibition of mediator release and enhancement of mediator action. Furthermore, the complete reversal of indomethacin potentiation of allergic inflammation by addition of PGE2 in low concentration advocates a regulatory function of the endogenous and locally formed PGE2. In the present in vivo model for mast cell-dependent inflammation the influence of PGE2 was mainly on the release of mediators. However, factors such as the degree of local blood flow, or the state of the tissue and the site of prostaglandin production, may in other instances shift the Yin-Yang balance in favour of PGE2 action at the target level for released mediators. Finally, it was noted that the cheek pouch mast cells, in addition to their pivotal role in the initiation of inflammatory reactions, have a predominant periarteriolar distribution that promotes oriented and, in terms of covered area, efficient migration of recruited leukocytes. Whether this previously unrecognized organization is specific for the hamster cheek pouch or exemplifies a more general phenomenon is presently not known.
Adv Prostaglandin Thromboxane Leukot Res 1989
PMID:Dual action of prostaglandin E2 in allergic inflammation. 252 34

The experiments discussed above indicate that during immediate hypersensitivity reactions, macrophages are stimulated by mast cells to synthesize PGE2 and 6-keto-PGF1 alpha but not LTC4. The arachidonic acid utilized for these products is mobilized from the macrophages itself and not shuttled from the mast cells. The stimulus for the involvement of the macrophage does not appear to be a direct cell interaction between the two cell types or a soluble factor released by the mast cells. Since the profile of eicosanoids produced by macrophages when exposed to mast cell granules is similar to that observed in the contribution of macrophages to immediate hypersensitivity reactions, mast cell granules appear to be responsible for the recruitment of macrophages to this reaction.
Adv Prostaglandin Thromboxane Leukot Res 1987
PMID:Nature of the mast cell-macrophage interaction in immediate hypersensitivity. 295 44

Antigen challenge of passively sensitized chopped human lung resulted in the generation of several arachidonic acid cyclooxygenase metabolites (AACM): thromboxane A2 (TxA2) as measured by its stable metabolite TxB2, prostaglandin D2 (PgD2), prostacyclin (PgI2) as measured by its stable metabolite 6-keto-PgF1 alpha, prostaglandin F2 alpha (PgF2 alpha), and prostaglandin E (PgE). The kinetics of AACM release after antigen challenge paralleled histamine release. All AACM were released in an antigen dose-dependent manner and reached maximal release at antigen concentrations lower than those required for maximal histamine release. Quantitatively, of the AACM measured, PgD2 and PgI2 were found to predominate in anaphylactic reactions of human lung parenchyma. Generation of PgD2 and PgI2 were 3- to 7-fold greater than that of other AACM measured. Thromboxane B2 was generated in quantities comparable to PgE and PgF2 alpha. Studies were designed to test the hypothesis that lung smooth muscle contraction per se can account for the generated AACM that are released during anaphylaxis of the lung. The studies compared antigen-induced AACM generation with methacholine-induced (10(-4) M) AACM generation. The failure to confirm this hypothesis was especially evident for PgD2 where release was dependent on mast cell activation. Thromboxane A2, PgD2, and PgI2 have been reported to have potent effects on smooth muscle. Our data suggested that these AACM are generated in such sufficient quantities that they may function in important aspects of the modulation of hypersensitivity responses in human lungs.
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PMID:Anaphylactic release of thromboxane A2, prostaglandin D2, and prostacyclin from human lung parenchyma. 617 Feb 42

Cardiac immediate hypersensitivity reactions in vitro are characterized by tachycardia, arrhythmias and coronary constriction. Whereas endogenous cardiac histamine release is responsible for the generation of arrhythmias, metabolites of arachidonic acid mediate the fall in coronary flow. In the present study, we have shown that antigenic challenge of sensitized guinea-pig hearts results in the release into the coronary effluent of immunoreactive thromboxane B2, 6-keto prostaglandin (PG) F1 alpha and PGF2 alpha. Thromboxane B2 was the predominant metabolite generated. After the administration of histamine (1-100 micrograms) or a partially purified preparation of slow-reacting substance of anaphylaxis (5-100 U) to the sensitized heart there was no detectable release of thromboxane B2 into the coronary effluent. After the administration of sodium arachidonate (3 X 10(-6) M) to the sensitized heart 40 min after antigenic challenge, there was a predominant release of 6-keto PGF1 alpha into the coronary effluent. Pretreatment of sensitized hearts with aspirin (5.5 X 10(-5) M), indomethacin (1.4 X 10(-5) M) or 1-(2-isopropylphenyl)imidazole (5.4 X 10(-5) M) resulted in inhibition of antigen-induced thromboxane B2 release and coronary vasoconstriction. These results suggest that during immediate hypersensitivity reactions, the coronary vasculature may be predisposed to ischemic and thrombotic episodes as a result of thromboxane release. Thromboxane formation occurs independently of the actions of histamine and slow-reacting substance of anaphylaxis and, since it is not generated preferentially by the coronary circulation of the sensitized heart in response to arachidonate infusion, it is plausible to suggest that it is of mast cell origin.
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PMID:Thromboxane and prostacyclin release during cardiac immediate hypersensitivity reactions in vitro. 689 66