Many patients with asthma are not fully controlled by currently available treatments and some of them display an airway remodeling leading to exaggerated decline of lung function. The aim of the present study was to unveil new mediators in asthma in order to better understand pathophysiology and propose or validate new potential therapeutic targets. A mouse model of asthma mimicking acute or chronic asthma disease was used to select genes undergoing a modulation in both acute and chronic conditions. Mice were exposed to ovalbumin during 1, 5 and 10 weeks (short, intermediate and long term model (ST, IT, LT)) and gene expression in the lung was studied using an Affymetrix^® 430 2.0 genome wide microarray and further confirmed by RT-PCR and immunohistochemistry for selected targets. We report that 598, 1406 and 117 genes were up-regulated and 490, 153, 321 down-regulated at ST, IT and LT, respectively. Genes related to mucous secretion displayed a progressively amplified expression during the allergen exposure protocol while genes corresponding to growth and differentiation factors, matrix metalloproteinases and collagens were mainly up-regulated at IT. By contrast, genes related to cell division were up-regulated at ST and IT and were down-regulated at LT. In this study, besides confirming that Arg1, Slc26a4, Ear11, Mmp12 genes are highly modulated throughout the asthma pathology, we show for the first time that Agr2, Scin and Cd209e genes are over-expressed throughout the allergen exposure and might therefore be considered as suitable new potential targets for the treatment of asthma.