{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,14]],"date-time":"2023-10-14T19:39:17Z","timestamp":1697312357053},"reference-count":34,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2007,5,17]],"date-time":"2007-05-17T00:00:00Z","timestamp":1179360000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2007,6]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Background\n\t\t\t\t\t<\/jats:bold> Tecastemizole, a major metabolite of astemizole, is a potent and selective H<jats:sub>1<\/jats:sub> receptor antagonist. Evidence suggests that this and certain other H<jats:sub>1<\/jats:sub> receptor antagonists may possess anti\u2010inflammatory effects that are, in some cases, independent of H<jats:sub>1<\/jats:sub> receptor antagonism.<\/jats:p><jats:p><jats:bold>Objective\n\t\t\t\t\t<\/jats:bold> The aim of this study was to investigate the anti\u2010inflammatory effects of tectastemizole in models of allergic inflammation.<\/jats:p><jats:p><jats:bold>Methods\n\t\t\t\t\t<\/jats:bold> Effects of tecastemizole were assessed in a murine model of allergic lung inflammation, in passive cutaneous anaphylaxis (PCA) responses in guinea\u2010pig skin and in <jats:italic>in vitro<\/jats:italic> assays measuring endothelial adhesion molecule expression and leucocyte\u2013endothelial adhesion.<\/jats:p><jats:p><jats:bold>Results\n\t\t\t\t\t<\/jats:bold> Tecastemizole inhibited antigen\u2010induced eosinophil recruitment to the lungs of allergic mice in a dose\u2010dependent manner. Furthermore, combination of a sub\u2010effective dose of tecastemizole, combined with a sub\u2010effective dose of dexamethasone inhibited eosinophil accumulation in this model. Plasma extravasation in PCA reactions was inhibited by tecastemizole, although by a mechanism that would appear to be H<jats:sub>1<\/jats:sub> receptor\u2010dependent. Cytokine\u2010induced endothelial intercellular adhesion molecule\u20101 and vascular cell adhesion molecule\u20101 expression, as well as mononuclear cell adhesion to human umbilical vein endothelial cells was inhibited by tecastemazole in a manner independent of H<jats:sub>1<\/jats:sub> receptor antagonism.<\/jats:p><jats:p><jats:bold>Conclusion\n\t\t\t\t\t<\/jats:bold> These data suggest that tecastemizole may have H<jats:sub>1<\/jats:sub> receptor\u2010independent effects in inhibiting late\u2010phase inflammatory responses, while acute responses appear to be inhibited in a H<jats:sub>1<\/jats:sub> receptor\u2010dependent manner. Furthermore, our data suggest an important potential steroid\u2010sparing role for such drugs in the treatment of allergic inflammatory conditions.<\/jats:p>","DOI":"10.1111\/j.1365-2222.2007.02730.x","type":"journal-article","created":{"date-parts":[[2007,5,17]],"date-time":"2007-05-17T23:56:29Z","timestamp":1179446189000},"page":"909-917","source":"Crossref","is-referenced-by-count":5,"title":["Effect of tecastemizole on pulmonary and cutaneous allergic inflammatory responses"],"prefix":"10.1111","volume":"37","author":[{"given":"R.","family":"Lever","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Hefni","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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