Mechanism of Airway Inflammation in Asthma
- 1 June 1993
- journal article
- review article
- Published by American Thoracic Society in American Review of Respiratory Disease
- Vol. 147 (6_pt_2) , S20-S24
- https://doi.org/10.1164/ajrccm/147.6_pt_2.s20
Abstract
Airway inflammation has emerged as an important contributor to mechanisms of asthma. Furthermore, the presence of airway inflammation is present even in the absence of severe symptoms. To study the mechanisms by which bronchial inflammation can occur in asthma, a number of models have been developed including the airway response to antigen in allergic subjects. The pattern that has emerged from such studies indicates prompt pulmonary mast-cell activation and the apparent initiation of an inflammatory response. This inflammatory response develops over hours and is important in the later and more persistent development of bronchial obstruction. The eosinophil is an important cell in this process as are proinflammatory cytokines generated from activated lung mononuclear cells. The consequence of this multiple cell, multiple proinflammatory product interaction is the establishment of a self-perpetuating, redundant process by which asthma severity increases.Keywords
This publication has 29 references indexed in Scilit:
- Predominant TH2-like Bronchoalveolar T-Lymphocyte Population in Atopic AsthmaNew England Journal of Medicine, 1992
- The Immunobiology of EosinophilsNew England Journal of Medicine, 1991
- Respiratory infections: Their role in airway responsiveness and the pathogenesis of asthmaJournal of Allergy and Clinical Immunology, 1990
- The eosinophil and bronchial asthma: Current understandingJournal of Allergy and Clinical Immunology, 1990
- Intercellular Adhesion Molecule-1 (ICAM-1) in the Pathogenesis of asthmaScience, 1990
- A New Approach to the Treatment of AsthmaNew England Journal of Medicine, 1989
- Mast cell lines produce lymphokines in response to cross-linkage of FcεRI or to calcium ionophoresNature, 1989
- Human eosinophils have prolonged survival, enhanced functional properties, and become hypodense when exposed to human interleukin 3.Journal of Clinical Investigation, 1988
- Tryptase Levels as an Indicator of Mast-Cell Activation in Systemic Anaphylaxis and MastocytosisNew England Journal of Medicine, 1987
- Inflammatory Mediators in Late Antigen-Induced RhinitisNew England Journal of Medicine, 1985