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 capacity of the beta 2-agonist terbutaline and the longer-acting beta 2-agonist formoterol to suppress the development of late phase skin reactions to anti-human IgE was evaluated in 17 healthy volunteers. Anti-IgE injected intradermally per se induced an early weal and flare reaction, followed by a progressively increasing induration, the LCR, with a duration of greater than or equal to 24 hr. The LCR was inhibited by 40% when the weal was infiltrated with formoterol 250 ng 30 min after challenge (n = 9, P less than 0.01). The same anti-LCR effect was achieved by compensating for the shorter duration of action of terbutaline with repeated drug infiltration in 12.5 micrograms doses of the weal produced by anti-IgE up to 3 1/2 hr after challenge (n = 8). The data support the hypothesis that beta 2-agonists, both short- and long-acting, inhibit IgE-dependent LCRs by preferentially interacting with inflammatory events after the initial mast cell degranulation.
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PMID:Inhibitory effects of formoterol and terbutaline on the development of late phase skin reactions. 134 58

Formoterol, a new beta 2-selective long-acting bronchodilator, was compared with terbutaline in terms of ability to inhibit dual phase skin reactions to anti-human IgE in volunteers. Anti-IgE induced an early wheal and flare reaction (WFR) followed by a progressively increasing induration, the late phase reaction (LCR), lasting greater than or equal to 24 h. Intradermal injection of formoterol 20 ng or terbutaline 500 ng 5 min before challenge gave equal inhibition of the WFR. The subsequent LCR was suppressed by formoterol (30%) for the whole 24 h period, while terbutaline only attenuated the first 4 h period. Increasing the dose range of both drugs 25-fold, caused a further analogous reduction of the WFR to anti-IgE. In this higher dose range formoterol (0.5 micrograms) antagonized the following 1-24 h LCR by 50%, while terbutaline (25 micrograms) only attenuated the LCR by an average of 20%, with higher effect in the first 6 h period. The anti-LCR capacity of formoterol was highly superior to that of terbutaline (P less than 0.001). The histamine-elicited wheal response was attenuated by both drugs, but they had no effect on the flare response, favouring an anti-permeability action of both compounds. The data support the concept that terbutaline, given locally in a single dose shortly before challenge, inhibits the mast cell mediator release reaction with limited consequences for the following LCR. In contrast to terbutaline, formoterol exerted a substantial anti-LCR action, probably by interfering with inflammatory mechanisms after the initial mast cell mediator release.
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PMID:Inhibition of anti-IgE induced skin response in normals by formoterol, a new beta 2-adrenoceptor agonist, and terbutaline. 2. Effect on the late phase reaction. 216 50