Asthma is a chronic disease associated with variable levels of airflow obstruction. Considerable evidence has been obtained to show that airway inflammation is a major factor in the pathogenesis of asthma in associated bronchial hyperresponsiveness, and in the level of disease severity. The inflammatory pattern in asthma is multicellular in nature, with mast cells, neutrophils, eosinophils, T lymphocytes, and epithelial cells participating in the response. Furthermore, it is known that mediators, cytokines, and chemokines from these cells contribute to the orchestration of the inflammatory process. Because airway inflammation appears to be a critical etiologic feature of asthma, it has become the target of therapy. In this review the features of airway inflammation will be examined, and the effect of therapeutic agents on markers of airway injury will be discussed. Establishing, understanding, and finally controlling the features of airway inflammation have given insight to disease pathogenesis and the effectiveness of various treatments. The integral role of inhaled corticosteroids in modifying the complex inflammatory component of asthma will be explored, with special focus on the high degree of efficacy associated with this treatment--vis-á-vis other therapeutic agents--in preventing or blocking specific proinflammatory markers.