Allergen-induced asthmatic responses: Relationship between increases in airway responsiveness and increases in circulating eosinophils, basophils, and their progenitors

P. G. Gibson, P. J. Manning, P. M. O'Byrne, A. Girgis-Gabardo, J. Dolovich, J. A. Denburg, F. E. Hargreave*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

The inflammatory response during allergen-induced asthma was assessed using serial measures of peripheral blood eosinophils (Eo), basophils (B), and Eo/B progenitor cells (Eo/B-CFU). A group of 14 stable asthmatic individuals (β2-agonists only as needed) had inhalation provocation tests with allergen (18 tests in total) and with diluent. Serial blood samples were taken before and 1 and 24 h after the tests; methylcellulose cultures for Eo/B-CFU and granulocyte-macrophage (GM-CFU) were scored at 14 days. Circulating Eo, B, and Eo/B-CFU were increased at 24 h after allergen inhalation when this resulted in increased histamine airway responsiveness (n = 13). In the 5 subjects with isolated early asthmatic responses the Eo, B, and Eo/B-CFU counts did not change. There was no change in the GM-CFU after allergen. The ratio change in circulating Eo/B-CFU was negatively correlated with baseline histamine airway responsiveness (r = -0.8, p < 0.05). Four subjects who had an isolated early response and no blood changes to one allergen developed an increase in histamine airway responsiveness and an increase in Eo, B, and Eo/B progenitors after inhalation of a second different allergen. The results indicate that in subjects with an allergen-induced increase in histamine airway responsiveness, an inflammatory response occurs that includes an increase in the number of Eo/B progenitors. This response, possibly mediated by Eo/B growth and differentiation factors, could lead to the accumulation of these cells in the airway and contribute to the airways inflammation present in asthma.

Original languageEnglish
Pages (from-to)331-335
Number of pages5
JournalAmerican Review of Respiratory Disease
Volume143
Issue number2
DOIs
Publication statusPublished - 1 Jan 1991
Externally publishedYes

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