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Unit of Respiratory
Medicine, Department of Medicine, University of Edinburgh, Royal
Infirmary, Edinburgh EH3 9YW, UK
Correspondence to: Professor W MacNee.
| The first 150 words of the full text of this article appear below. |
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Introduction |
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Acute and chronic alveolar and/or bronchial inflammation is
thought to be central to the pathogenesis of many lung disorders such
as asthma, chronic obstructive pulmonary disease (COPD), adult
respiratory distress syndrome (ARDS), and idiopathic pulmonary fibrosis
(IPF). The site and specific characteristics of the inflammatory responses may be different in each of these diseases, but all are
characterised by the recruitment to the lungs and activation of immune
and inflammatory cells. These activated cells produce cytokines,
oxidants and many other mediators which are involved in
inflammation.1 2 Recent data indicate that, in addition, airway epithelial cells are able to act as immune effector cells by
secreting pro-inflammatory mediators, oxidants, and
cytokines.3 Once triggered, an inappropriate chronic
inflammatory response persists in these conditions and is presumed to
result in lung injury. The intracellular molecular mechanisms in
response to environmental signals, leading to increased gene expression
and biosynthesis of proinflammatory mediators by airspace
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W. MACNEE and I. RAHMAN Oxidants and Antioxidants as Therapeutic Targets in Chronic Obstructive Pulmonary Disease Am. J. Respir. Crit. Care Med., November 1, 1999; 160(5): S58 - 65. [Abstract] [Full Text] [PDF]
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