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

Julie A. Swartzendruber, Adam J. Byrne, Paul J. Bryce*

*Corresponding author for this work

Research output: Contribution to journalArticle

8 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)536-540
Number of pages5
JournalJournal of Immunology
Volume188
Issue number2
DOIs
StatePublished - Jan 15 2012

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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