Introduction
In recent years attention has been focused on the inflammatory nature of the airway mucosa in patients with bronchoconstriction and asthma. Tho key questions have been raised. First, is this inflammation unique to asthma and, if so, what characterizes "asthmatic" inflammation? Second, what is the relationship of airway inflammation to the physiologic progression of the disease that is expressed as bronchial hyperresponsiveness? The purpose of the Roundtable Discussion, which was chaired by Dr. K. Frank Austen, was to address these questions, to attempt to define the nature of the inflammatory process seen in asthmatic airways. The starting point for the discussion was a review of the pathology of asthma based on findings from fatal asthma as well as on data from bronchoalveolar lavagesand biopsies. This was followed by a detailed analysis of the cellular
AM REV RESPIR DIS 1992; 145:S1
basis of the disease in terms of the constitutive elements (epithelium, fibroblasts, endothelial cells, mast cells) and the infiltrating cells(CD+T-cells, eosinophils, macrophages). The relationship between these inflammatory components and bronchial hyperresponsivenesswas examined, and the contributions of platelet-activating factor, sulfidopeptide leukotrienes, mast cell neutral proteases, microvasculature, IgE, and neurogenic mechanisms were addressed with this in mind. The meeting concluded with a discussion of the implications of asthmatic inflammation for the treatment of asthmatic patients. Apart from the formal presentations, which contained exciting and novel data, one of the highlights of the Roundtable was the extensive discussion. As with all successful workshops, the faculty raised more questions than it answered. In editing the proceedings of the
meeting, I have tried to retain the content and flavor of the incisive issues raised. I hope that readers will enjoy reading this supplement as much as the faculty enjoyed participating in the Roundtable Discussion. TAK
H. LEE, M.D.
Department of Allergy and Allied Respiratory Disorders Guy's Hospital London, United Kingdom
The editor, chairperson, and participants are grateful to Dr. Judith Rosen Farrar for her help assisting withthe publication and coordination of the Roundtable Discussions and to Fisons Pharmaceuticals, USA, for sponsoring the meeting.
S1
In recent years attention has been focused on the inflammatory nature of the airway mucosa in patients with bronchoconstriction and asthma. Tho key questions have been raised. First, is this inflammation unique to asthma and, if so, what characterizes "asthmatic" inflammation? Second, what is the relationship of airway inflammation to the physiologic progression of the disease that is expressed as bronchial hyperresponsiveness? The purpose of the Roundtable Discussion, which was chaired by Dr. K. Frank Austen, was to address these questions, to attempt to define the nature of the inflammatory process seen in asthmatic airways. The starting point for the discussion was a review of the pathology of asthma based on findings from fatal asthma as well as on data from bronchoalveolar lavagesand biopsies. This was followed by a detailed analysis of the cellular
AM REV RESPIR DIS 1992; 145:S1
basis of the disease in terms of the constitutive elements (epithelium, fibroblasts, endothelial cells, mast cells) and the infiltrating cells(CD+T-cells, eosinophils, macrophages). The relationship between these inflammatory components and bronchial hyperresponsivenesswas examined, and the contributions of platelet-activating factor, sulfidopeptide leukotrienes, mast cell neutral proteases, microvasculature, IgE, and neurogenic mechanisms were addressed with this in mind. The meeting concluded with a discussion of the implications of asthmatic inflammation for the treatment of asthmatic patients. Apart from the formal presentations, which contained exciting and novel data, one of the highlights of the Roundtable was the extensive discussion. As with all successful workshops, the faculty raised more questions than it answered. In editing the proceedings of the
meeting, I have tried to retain the content and flavor of the incisive issues raised. I hope that readers will enjoy reading this supplement as much as the faculty enjoyed participating in the Roundtable Discussion. TAK
H. LEE, M.D.
Department of Allergy and Allied Respiratory Disorders Guy's Hospital London, United Kingdom
The editor, chairperson, and participants are grateful to Dr. Judith Rosen Farrar for her help assisting withthe publication and coordination of the Roundtable Discussions and to Fisons Pharmaceuticals, USA, for sponsoring the meeting.
S1
