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Mechanisms of Inflammation and Potential Role in the Pathogenesis of Asthma

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Abstract:

Neurogenic inflammation produces potent responses in multiple cells in the airways. These responses normally are limited by the presence on the surface of target cells of neutral endopeptidase (NEP), an enzyme that cleaves and inactivates neuropeptides that come in close contact with the cell and thereby limits neurogenic inflammatory responses. Inhibition of NEP by drugs, respiratory viruses, cigarette smoke, and toluene diisocyanate result in exaggerated neurogenic responses, while upregulation of NEP (e.g., by corticosteroids) may suppress the responses. Exogenously delivered recombinant human NEP also inhibits the responses.

The novel system whereby sensory nerve stimulation results in the release of inflammatory neuropeptides provides a potentially important mechanism in the pathogenesis of airway inflammation. The strategies discussed here provide tools for the investigation of this system and suggests methods for therapeutic intervention.

Document Type: Research Article

DOI: https://doi.org/10.2500/108854191779011774

Publication date: 1991-03-01

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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