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Asthma is a complex genetic disease that is under the influence of many genes, and it has been proposed that different genes act in different families and different individuals. The aim of the present study was to investigate at the genomic level the genes that may participate in the causation and origins of asthma using microarray technology. A better understanding of these processes has the potential to identify markers of disease and new therapeutic targets. Seven atopic asthmatics and five non-asthmatics underwent bronchoscopy to obtain bronchial biopsies. Total RNA was purified from bronchial biopsies, and biotynilated complementary RNA was prepared and hybridized to Affymetrix Hum 133 two plus chips (Affymetrix, Santa Clara CA). Using the multi-chip average procedure, we compared the mRNA expression profiles of 47,000 genes and/or EST sequences of atopic asthmatic with normal controls. Four hundred eighty genes had twofold mean regulation expression differences or greater. Three hundred fifty-two genes were upregulated, including surface molecules involved in T- cell and B-cell activation, cytokines, extracellular matrix proteins, intracellular signaling products, and transcription factors. In conclusion, atopic asthmatics show a number of activated proinflamatory pathways that participate in T- and B-cell activation and airway remodeling. These differentially expressed genes identify potential molecular targets for preventive and therapeutic options in asthma.