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This Article Full Text Full Text (PDF) Supplemental Figures and Tables All Versions of this Article: 38/3/303    most recent 00057.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Camateros, P. Articles by Radzioch, D. PubMed PubMed Citation Articles by Camateros, P. Articles by Radzioch, D.

Modulation of the allergic asthma transcriptome following resiquimod treatment

¹ Department of Medicine, Division of Experimental Medicine, McGill University, Montréal, Québec
² Montreal General Hospital Research Institute, Montréal, Québec
³ Department of Human Genetics, McGill University, Montréal, Québec
⁴ McGill University and Génome Québec Innovation Centre, Montréal, Québec
⁵ Ontario Institute for Cancer Research, Toronto, Ontario, Canada

Resiquimod is a compound belonging to the imidazoquinoline family of compounds known to signal through Toll-like receptor 7. Resiquimod treatment has been demonstrated to inhibit the development of allergen induced asthma in experimental models. The aim of the present study was to elucidate the molecular processes that were altered following resiquimod treatment and allergen challenge in a mouse model of allergic asthma. Employing microarray analysis, we have characterized the "asthmatic" transcriptome of the lungs of A/J and C57BL/6 mice and determined that it includes genes involved in the control of cell cycle progression, the complement and coagulation cascades, and chemokine signaling. Our results demonstrated that resiquimod treatment resulted in the normalization of the expression of genes involved with airway remodeling, and generally, chemokine signaling. Resiquimod treatment also altered the expression of cell adhesion molecules, and molecules involved in natural killer (NK) cell-mediated cytotoxicity. Furthermore, we have demonstrated that systemic resiquimod administration resulted in the recruitment of NK cells to the lungs and livers of the mice, although no causal relationship between NK cell recruitment and treatment efficacy was found. Overall, our findings identified several genes, important in the development of asthma pathology, that were normalized following resiquimod treatment, thus improving our understanding of the molecular consequences of resiquimod treatment in the lung milieu. The recruitment of NK cells to the lungs may also have application in the treatment of virally induced asthma exacerbations.

S28463; R-848; Toll-like receptor 7; microarray