At present, general consensus exits on the inflammatory nature of bronchial asthma. Advances in the knowledge of pathogenetic mechanisms of bronchial asthma are certainly to be ascribed to the use of immunobiological, molecular and genetic approaches for studying experimental models and human bronchial asthma. The histopathological hallmark of bronchial asthma consists in the constant presence, at the level of bronchial mucosa, even in the mild and intermittent syndromes, of epithelial lesions, thickening of basement membrane, and inflammatory infiltration consisting of activated eosinophils, Th2 lymphocytes and degranulated mast cells. Cellular and molecular alterations responsible for this typical bronchial inflammation and the subsequent patho-physiological and clinical characteristics of bronchial asthma have been identified. It has been shown that interleukin-4 is the principal cytokine necessary for Th2 lymphocyte differentiation and expansion and IgE production. Interleukin-5 acts specifically on eosinophil activation, terminal differentiation, and survival. As only eosinophils primed by interleukin-5 as well as by interleukin-3 and granulocyte macrophage-colony stimulating factor can express all the membrane receptors and integrins, they become able to bind to adhesion molecules overexpressed on the mucosal microvascular endothelial cells and of being selectively chemoattracted by a particular subgroup of beta-chemokines, which bind to their membrane CC-receptor-3. The amplification and maintenance of airway inflammation and the clinical exacerbations and chronicity of bronchial asthma depend on complex mechanisms. Tumor necrosis factor-alpha and interleukin-1 beta play a fundamental role in the induction of multiple cellular and molecular interactions. Molecular approaches are now being used to define genetic predisposition. Candidate genes have been located on different chromosomes. In addition to bronchodilator medication to relieve symptoms, the most important purpose of asthma therapy must be based on anti-inflammatory agents to reduce airway inflammation and airway hyperreactivity. Corticosteroids appear able to interfere with almost all components of inflammation. New inhaled steroids have radically modified therapeutic principles of bronchial asthma. Even cromones and anti-leukotrienes have been recommended as anti-inflammatory agents. Some developing therapeutic strategies involve use of anti-IgE antibodies, interleukin-4 and interleukin-5 inhibitors and chemokine receptor antagonists.