Asthma is a multifactorial and complex respiratory disorder where a chronic inflammatory process of the airways occurs. As for studies undertaken by researchers in our group, the expression of COX-2 levels in the nasal mucosa of asthmatics is clearly reduced. Regulatory abnormalities of COX-2 can lead to disruptions of inflammations. In the same patients, a parallel reduced expression of the COX-2 transcription factor NFkB has been observed. In addition, PGE2, one of the enzyme's product, is know to exert a modulation of the respiratory function. These and other data allow us to establish the following hypothesis: changes in the expression of COX-2 driven by an abnormal regulation of the enzyme, do correlate with changes in the bronchial reactivity and the lung inflammation. Given the ethical and technical barriers to research on human patients, experimental models are required to further into the pathophysiological mechanisms in asthma. Mice asthma models are very valuable to investigate the activity of COX-2 in the lower airways and the lung parenchyma along the course of the disease. The objectives of our proposal are: 1) study the relevance of COX-2 to bronchial hyperreactivity and inflammation in asthmatic mice. 2) assess the potential abnormalities in the regulation of the expression of COX-2 in asthmatic mice (determination of NF-kB, IkB-\alpha and IkB-\beta).
|Effective start/end date||29/11/03 → 28/11/06|