| First Author | Swartzendruber JA | Year | 2012 |
| Journal | J Immunol | Volume | 188 |
| Issue | 2 | Pages | 536-40 |
| PubMed ID | 22156496 | Mgi Jnum | J:181123 |
| Mgi Id | MGI:5308846 | Doi | 10.4049/jimmunol.1101795 |
| Citation | Swartzendruber JA, et al. (2012) Cutting edge: histamine is required for IL-4-driven eosinophilic allergic responses. J Immunol 188(2):536-40 |
| abstractText | 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. |
