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.