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J Immunol. 2012 Jan 15;188(2):536-40. doi: 10.4049/jimmunol.1101795. Epub 2011 Dec 9.

Cutting edge: histamine is required for IL-4-driven eosinophilic allergic responses.

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  • 1Division of Allergy-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.

Abstract

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-driven 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.

PMID:
22156496
[PubMed - indexed for MEDLINE]
PMCID:
PMC3261133
Free PMC Article
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