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Mediators of Inflammation
Volume 10 (2001), Issue 3, Pages 143-154
http://dx.doi.org/10.1080/09629350124877

Inflammatory cell distribution in guinea pig airways and its relationship to airway reactivity

1Department of Molecular Pharmacology, University Centre for Pharmacy, A. Deusinglaan 1, Groningen 9713 AV, The Netherlands
2Department of Pathology and Laboratory Medicine, University Hospital Groningen, Hanzeplein 1, Groningen 9713 GZ, The Netherlands

Copyright © 2001 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Although airway inflammation and airway hyperreactivity are observed after allergen inhalation both in allergic humans and animals, little is known about the mechanisms by which inflammatory cells can contribute to allergen-induced airway hyperreactivity. To understand how inflammatory cell infiltration can contribute to airway hyperreactivity, the location of these cells within the airways may be crucial.

Using a guinea pig model of acute allergic asthma, we investigated the inflammatory cell infiltration in different airway compartments at 6 and 24 h (i.e. after the early and the late asthmatic reaction, respectively) after allergen or saline challenge in relation to changes in airway reactivity (AR) to histamine.

At 6 h after allergen challenge, a threefold (p<0.01) increase in the AR to histamine was observed. At 24 h after challenge, the AR to histamine was lower, but still significantly enhanced (1.6-fold, p<0.05).

Adventitial eosinophil and neutrophil numbers in both bronchi and bronchioli were significantly increased at 6 h post-allergen provocation as compared with saline (p<0.01 for all), while there was a strong tendency to enhanced eosinophils in the bronchial submucosa at this time point (p=0.08). At 24 h after allergen challenge, the eosinophilic and neutrophilic cell infiltration was reduced. CD3+ T lymphocytes were increased in the adventitial compartment of the large airways (p<0.05) and in the parenchyma (p<0.05) at 24h post-allergen, while numbers of CD8+ cells did not differ from saline treatment at any time point post-provocation.

The results indicate that, after allergen provocation, inflammatory cell numbers in the airways are mainly elevated in the adventitial compartment. The adventitial inflammation could be important for the development of allergen-induced airway hyperreactivity.