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Role of prostaglandin D 2 /CRTH2 pathway on asthma exacerbation induced by A spergillus fumigatus
Author(s) -
Liu Haixia,
Zheng Mingrui,
Qiao Jianou,
Dang Yajie,
Zhang Pengyu,
Jin Xianqiao
Publication year - 2014
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12234
Subject(s) - aspergillus fumigatus , prostaglandin d2 , immunology , ovalbumin , eosinophilia , eosinophil , exacerbation , medicine , asthma , inflammation , allergic inflammation , receptor , immune system
Summary A spergillus fumigatus is often associated in asthmatic patients with the exacerbation of asthma symptoms. The pathomechanism of this phenomenon has not been fully understood. Here, we evaluated the immunological mechanisms and the role of the prostaglandin D 2 / Chemoattractant Receptor‐Homologous Molecule Expressed on Th2 Cells (CRTH2) pathway in the development of Aspergillus ‐associated asthma exacerbation. We studied the effects of A . fumigatus on airway inflammation and bronchial hyper‐responsiveness in a rat model of chronic asthma. Inhalation delivery of A . fumigatus conidia increased the airway eosinophilia and bronchial hyper‐responsiveness in ovalbumin‐sensitized, challenged rats. These changes were associated with prostaglandin D 2 synthesis and CRTH 2 expression in the lungs. Direct inflammation occurred in ovalbumin‐sensitized, challenged animals, whereas pre‐treatment with an antagonist against CRTH 2 nearly completely eliminated the A . fumigatus ‐induced worsening of airway eosinophilia and bronchial hyper‐responsiveness. Our data demonstrate that production of prostaglandin D 2 followed by eosinophil recruitment into the airways via a CRTH 2 receptor are the major pathogenic factors responsible for the A . fumigatus ‐induced enhancement of airway inflammation and responsiveness.