{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,3,28]],"date-time":"2025-03-28T04:06:08Z","timestamp":1743134768002,"version":"3.40.3"},"reference-count":33,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2012,1,1]],"date-time":"2012-01-01T00:00:00Z","timestamp":1325376000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,1,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Histamine is an important allergic mediator, and studies have defined roles for both histamine 1 and 4 receptors in allergic airway inflammation. In this study, we show that histamine is necessary to generate IL-4\u2013driven eosinophilic inflammation, as histamine-deficient mice cannot generate eosinophilic lung inflammation in response to intratracheal IL-4 and exogenous histamine restores responsiveness. This is histamine 2 receptor (H2R) dependent because H2R knockout mice fail to respond to IL-4, and a H2R agonist restores inflammation in histidine decarboxylase knockout. Furthermore, alveolar epithelial cells require H2R to produce CCL24, an eosinophil recruitment factor, whereas H2R blockade reduces CCL24 production from wild-type cells. In an allergic inflammation model, H2R knockout mice show significantly reduced eosinophilic inflammation and CCL24 expression. These data demonstrate a previously unidentified role for H2R in allergic inflammation and establishes a synergy between endogenous histamine and IL-4 that supports eosinophilic recruitment to the lung.<\/jats:p>","DOI":"10.4049\/jimmunol.1101795","type":"journal-article","created":{"date-parts":[[2011,12,10]],"date-time":"2011-12-10T05:29:48Z","timestamp":1323494988000},"page":"536-540","source":"Crossref","is-referenced-by-count":9,"title":["Cutting Edge: Histamine Is Required for IL-4\u2013Driven Eosinophilic Allergic Responses"],"prefix":"10.1093","volume":"188","author":[{"given":"Julie A","family":"Swartzendruber","sequence":"first","affiliation":[{"name":"Division of Allergy-Immunology, Feinberg School of Medicine, Northwestern University , Chicago, IL 60611"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Adam J","family":"Byrne","sequence":"additional","affiliation":[{"name":"Division of Allergy-Immunology, Feinberg School of Medicine, Northwestern University , Chicago, IL 60611"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul J","family":"Bryce","sequence":"additional","affiliation":[{"name":"Division of Allergy-Immunology, Feinberg School of Medicine, Northwestern University , Chicago, IL 60611"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2012,1,15]]},"reference":[{"key":"2025032409462260600_r1","doi-asserted-by":"crossref","first-page":"7","DOI":"10.1016\/S1074-7613(02)00332-1","article-title":"IL-4 induces characteristic Th2 responses even in the combined absence of IL-5, IL-9, and IL-13","volume":"17","author":"Fallon","year":"2002","journal-title":"Immunity"},{"key":"2025032409462260600_r2","doi-asserted-by":"crossref","first-page":"7821","DOI":"10.1073\/pnas.93.15.7821","article-title":"Phenotypic and physiologic characterization of transgenic mice expressing interleukin 4 in the lung: lymphocytic and eosinophilic inflammation without airway hyperreactivity","volume":"93","author":"Rankin","year":"1996","journal-title":"Proc. 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