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IMIQUIMOD, A TOLL‐LIKE RECEPTOR 7 LIGAND, INHIBITS AIRWAY REMODELLING IN A MURINE MODEL OF CHRONIC ASTHMA
Author(s) -
Du Qiang,
Zhou LinFu,
Chen Zhen,
Gu XiaoYan,
Huang Mao,
Yin KaiSheng
Publication year - 2009
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2008.05027.x
Subject(s) - ovalbumin , imiquimod , medicine , immunology , bronchoalveolar lavage , inflammation , asthma , immunoglobulin e , airway , transforming growth factor , immune system , lung , antibody , surgery
SUMMARY1 Imiquimod, a synthetic Toll‐like receptor (TLR) 7 ligand, has been shown to attenuate airway inflammation and airway hyperresponsiveness (AHR) in acute murine models of allergic asthma. In the present study, we investigated the effect of imiquimod on allergen‐induced airway remodelling in chronic experimental asthma. 2 Ovalbumin (OVA)‐sensitized mice were chronically challenged with aerosolized OVA for 8 weeks. Some mice were exposed to an aerosol of 0.15% imiquimod daily during the period of OVA challenge. Twenty‐four hours after the last OVA challenge, mice were evaluated for the development of airway inflammation, AHR and airway remodelling. The levels of total serum IgE and Th2 cytokines (interleukin (IL)‐4, IL‐5 and IL‐13) in bronchoalveolar lavage fluid (BALF) and the expression of transforming growth factor (TGF)‐β1 protein in lungs were measured by ELISA and immunohistochemistry, respectively. 3 The results demonstrated that imiquimod significantly inhibited chronic inflammation, persistent AHR and airway remodelling in chronic experimental asthma. In addition, imiquimod reduced levels of total serum IgE and BALF Th2 cytokines and diminished expression of TGF‐β1 in remodelled airways. 4 In summary, the results of the present study indicate that imiquimod may attenuate the progression of airway inflammation and remodelling, providing potential in the treatment of asthma.