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

Citation
F. Westerhof et al., Inflammatory cell distribution in guinea pig airways and its relationship to airway reactivity, MEDIAT INFL, 10(3), 2001, pp. 143-154
Citations number
71
Categorie Soggetti
Immunology
Journal title
MEDIATORS OF INFLAMMATION
ISSN journal
09629351 → ACNP
Volume
10
Issue
3
Year of publication
2001
Pages
143 - 154
Database
ISI
SICI code
0962-9351(200106)10:3<143:ICDIGP>2.0.ZU;2-J
Abstract
ALTHOUGH airway inflammation and airway hyperreactivity are observed after allergen inhalation both in allergic humans and animals, little is known ab out the mechanisms by which inflammatory cells can contribute to allergen-i nduced airway hyperreactivity. To understand how inflammatory cell infiltra tion 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 infl ammatory cell infiltration in different airway compartments at 6 and 24 h ( i.e. after the early and the late asthmatic reaction, respectively) after a llergen 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 bronchiol i 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 enhan ced eosinophils in the bronchial submucosa at this time point (p = 0.08). A t 24 h after allergen challenge, the eosinophilic and neutrophilic cell inf iltration was reduced. CD3(+) T lymphocytes were increased in the adventiti al 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 fro m saline treatment at any time point post-provocation. The results indicate that, after allergen provocation, inflammatory cell nu mbers in the airways are mainly elevated in the adventitial compartment. Th e adventitial inflammation could be important for the development of allerg en-induced airway hyperreactivity.