Asthma is a common clinical entity ,yet its pathophysiological mechanism remains poorly understood. NF-κB transcription factors regulate a plethora of genes essential to innate immunity and inflammation. Several lines of evidence suggest that NF-κB also plays a central role in the pathogenesis of asthma. Naf1(ABIN-1) is an intracellular protein that has the potential to inhibit NF-κB activation upon overexpression. Study in vitro suggested that ooexpression of Naf1 site-specific mutants(Q 463→E 463 ,Q 464→E 464) interferes in a dominant negative manner with the NF-κB inhibiting function of wild type Naf1.To test the role of Naf1-mut in vivo we generate the pCMV- Tag 3B/Naf1-mut transgenic mouse . Our experiments is to detect various parameters in a murine model of allergen induced asthma compared to background mouse C57. Overexpresssion of Naf1-mut results in a considerable reduction of allergen-induced eosinophil infiltration into the lungs. This is associated with a significant reduction of eotaxin, interleukin-4, and interleukin-5 in bronchoalveolar lavage fluid. But it is not in line with an increase of immunoglobulin E levels in serum. |