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Immunological Aspects of Chronic Asthma

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Abstract:

The demonstration of leucocyte activation in the peripheral blood of patients with chronic asthma together with elevated levels of neutrophil chemotactic activity provides evidence for an underlying inflammatory process in asthma and confirms that bronchial inflammation is an important cause of airways obstruction. Corticosteroids may act through a variety of mechanisms but their anti-inflammatory action is probably mediated, at least in part, through the inhibition of phospholipase A2. Corticosteroids suppress leucocyte activation in asthma and this is associated with an improvement in lung function, thus supporting the view that their anti-inflammatory mode of action is of essential importance. However, a small group of chronic asthmatics do not respond to corticosteroids, even when given in large doses and the nature of the cellular defect in these "corticosteroid-resistant" individuals is thought to be the monocyte. The cells of the monocyte/macrophage series may play a central role in the pathogenesis of chronic asthma.

Document Type: Research Article

DOI: https://doi.org/10.2500/108854187779023541

Publication date: 1987-09-01

More about this publication?
  • Allergy and Asthma Proceedings is a peer reviewed publication dedicated to distributing timely scientific research regarding advancements in the knowledge and practice of allergy, asthma and immunology. Its primary readership consists of allergists and pulmonologists.

    The goal of the Proceedings is to publish articles with a predominantly clinical focus which directly impact quality of care for patients with allergic disease and asthma.

    Featured topics include asthma, rhinitis, sinusitis, food allergies, allergic skin diseases, diagnostic techniques, allergens, and treatment modalities. Published material includes peer-reviewed original research, clinical trials and review articles.

    Articles marked "F" offer free full text for personal noncommercial use only.

    The journal is indexed in Thomson Reuters Web of Science and Science Citation Index Expanded, plus the National Library of Medicine's PubMed service.
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