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Am. J. Respir. Cell Mol. Biol., Volume 20, Number 5, May, 1999 992-1000

alpha 4 Integrin-Dependent Eotaxin Induction of Bronchial Hyperresponsiveness and Eosinophil Migration in Interleukin-5 Transgenic Mice

Takeshi Hisada, Paul G. Hellewell, Mauro M. Teixeira, Monika G. K. Malm, Michael Salmon, Tung-Jung Huang, and K. Fan Chung

National Heart and Lung Institute at Imperial College School of Medicine, London, United Kingdom

We investigated the roles of eosinophil infiltration and activation induced by the eosinophil-selective chemokine eotaxin, and of the expression of eosinophil alpha 4 and beta 2 integrins in causing bronchial hyperresponsiveness (BHR) in interleukin (IL)-5 CBA/Ca transgenic mice. These mice did not show BHR, despite the presence of some eosinophils in the lungs. Intratracheal mouse recombinant eotaxin (3 µg) did not induce BHR in wild-type mice. In IL-5 transgenic mice, eotaxin (3 and 5 µg) increased responsiveness at 24 h and increased eosinophils in bronchoalveolar lavage (BAL) fluid by 9.4- and 14-fold by 24 h, respectively, together with augmentation of eosinophil peroxidase activity and eosinophil infiltration in the airway submucosa. Using flow cytometry, the expression of alpha 4, CD11b, and CD18 was upregulated in BAL, but not in blood, eosinophils. A rat anti-alpha 4 antibody inhibited eotaxin-induced BHR and eosinophil migration and activation, but an anti-CD11b antibody had no significant effects on BHR. A combination of both antibodies was more effective. IL-5 and eotaxin synergize in the induction of BHR and airway eosinophilia, effects that are dependent on the induction of eosinophil alpha 4 integrin. Expression of BHR depends on the recruitment and activation of eosinophils.




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