Display Settings:


Send to:

Choose Destination
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
Clin Exp Allergy. 1998 Jun;28 Suppl 2:11-6.

Mechanisms of mucosal inflammation in the nose and lungs.

Author information

  • Upper Respiratory Medicine, Imperial College School of Medicine, at National Heart and Lung Institute, London, UK.


The early inflammatory response during allergic rhinitis and asthma is associated with IgE-mediated mast cell activation and resultant release of primary inflammatory mediators. The late phase reaction is characterized by recruitment, activation and tissue infiltration of leucocyte populations, including T lymphocytes, eosinophils, basophils and neutrophils. T helper type 2 CD4+ cells, a T lymphocyte subset with a distinctive cytokine profile, are thought to regulate the recruitment and activation of other effector cells. This review discusses the results of studies conducted under experimental and natural conditions of allergen exposure, which confirm the presence of eosinophilia, changes in lymphocyte populations, and increased expression of a TH2-cytokine profile in the nasal mucosa following allergen-induced rhinitis, and the alleviation of both clinical symptoms and inflammatory responses by prior treatment with topical fluticasone propionate. Similar effects are demonstrated to occur in the lower airway following allergen challenge in asthma patients, and to be ameliorated by oral corticosteroid therapy. These studies add weight to the argument that asthma and rhinitis share a common pathophysiology characterized by similar inflammatory events, and should both benefit from early preventative treatment with topical corticosteroids.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Blackwell Publishing
    Loading ...
    Write to the Help Desk