[Physiopathology of asthma]

Asthma is a multifactorial disease where genetic predisposition, environmental factors (allergens and pollutants) and endogenous factors intervene to varying degrees. Among the disturbances involved in the physiopathology of asthma dysfunction of the autonomic nervous system and development of bronchial inflammation are now known to play the major roles. From the adrenergic system, the role of which is now controverted, the attention of pharmacologists has shifted to the cholinergic central nervous system responsible for bronchial tone and the non adrenergic non cholinergic (NANC) nervous system. The more recently known NANC system is complex and mediated by neuropeptides, and it can alternately induce bronchodilatation and bronchoconstriction, as well as vasoconstriction and vasodilatation. The inhibitory NANC system acts through the bronchodilator VIP. The excitatory NANC system is mediated by tachykinins as which are potent bronchoconstrictors. Interaction of this system with the inflammatory cells induces a "neurogenic inflammation". Local inflammatory reaction is an almost constant element of asthma, irrespective of the cause of the disease. Although mast cells are the initial cells of the inflammatory reaction, there are important and complex cellular interactions with eosinophils, macrophages, lymphocytes and epithelial cells. Owing to their direct cytotoxic actions on the bronchial epithelium, eosinophils play a key-role in the inflammatory reaction. Cytokines secreted by alveolar macrophages, lymphocytes and mast cells amplify and maintain the inflammatory process.