This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Vondracek, T. G. Articles by Stanaszek, W. F. Search for Related Content Social Bookmarking                         What's this?

The Pathophysiology of Asthma

Walter F. Stanaszek

Atopy predisposes an individual to the development of asthma, whereby specific triggers may repeatedly cause acute exacerbations and contribute to chronic inflammation. This IgE-mediated response to common allergens is the strongest predisposing factor for developing asthma. Airway inflammation involves release of immunological mediators via T lymphocyte dependent, and IgE dependent and independent mechanisms which attract inflammatory cells from the circulation. The role of the eicosanoids as pivotal mediators in promoting some of the changes in asthma has only recently been fully explored. Inflammatory reactions result when mediators and cytokines released from resident and infiltrating cells interact. This interaction also contributes to the bronchoconstriction, hypersecretion, and mucosal edema in the airways.

Journal of Pharmacy Practice, Vol. 10, No. 3, 176-185 (1997)
DOI: 10.1177/089719009701000308


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?