The New Gestalt: Asthma as a Chronic Inflammatory Disease

Abstract

A general appreciation of the role of chronic inflammation in the immunopathogenesis of bronchial asthma is long overdue. The consequence of this new gestalt will be a renaissance in basic research, drug development, and treatment, the focus of which will be aimed at understanding and ameliorating the causes rather than just the symptoms of chronic asthma. The recent “rediscovery” and “reinterpretation” of the histopathologic features of chronic asthma, the careful definition of the tissue, cellular, and humoral events integral to the development of chronic bronchopulmonary inflammation, and the demonstration that chronic asthma possesses many features of recurrent late-phase reactions, has provided the basis for models and testable hypotheses of the complex cellular and humoral networks involved. The model proposed by Professor A. B. Kay, in this issue of the Journal of Asthma provides just such a framework for further elucidation of the role of inflammatory cells and their soluble mediators in bronchial asthma, specifically focusing on the possibility of a central role for “chronically activated” T helper cells, T-cell-derived lymphokines, and eosinophils in the chronic pathology of this disorder.