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Infection and Immunity, September 1998, p. 4425-4430, Vol. 66, No. 9
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

An Essential Role for Interleukin-5 and Eosinophils in Helminth-Induced Airway Hyperresponsiveness

Laurie R. Hall,1 Rajeev K. Mehlotra,1 Alan W. Higgins,1 Musa A. Haxhiu,2 and Eric Pearlman1,*

Divisions of Geographic1 and Pulmonary2 Medicine, Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106

Received 25 March 1998/Returned for modification 14 May 1998/Accepted 4 June 1998

Infection with the parasitic helminth Brugia malayi can result in development of a severe asthmatic response termed tropical pulmonary eosinophilia. This disease, thought to result from a host inflammatory response to blood parasites which become trapped in the lung microvasculature, is characterized by a profound eosinophilic infiltration into the lungs. Recruitment of eosinophils also correlates with the development of airway hyperresponsiveness (AHR) to cholinergic agonists and severe asthmatic symptoms. Our studies examined the role of interleukin-5 (IL-5) in helminth-induced pulmonary eosinophilia and AHR. C57BL/6 mice immunized with killed B. malayi microfilariae and challenged intravenously with live microfilariae exhibit many of the characteristics of human disease, including peripheral and pulmonary eosinophilia. Cells recovered by bronchoalveolar lavage of sensitized mice consisted of 3.8% eosinophils on day 1 postchallenge and 84% on day 10. Extracellular major basic protein was present on the surface of airway epithelial cells as early as day 1 and continued to be evident after 8 days, indicating sustained activation and degranulation of eosinophils in the lung. These histologic changes correlated with the development of AHR to carbachol. In contrast to immunocompetent mice, immunization and challenge with B. malayi in IL-5-/- mice did not induce peripheral or pulmonary eosinophilia, and these mice failed to show AHR in response to cholinergic agonists. Taken together, these data indicate that IL-5 and eosinophils are required for the induction of AHR by filarial helminths.

* Corresponding author. Mailing address: Division of Geographic Medicine, Case Western Reserve University School of Medicine, W137, 2109 Adelbert Road, Cleveland, OH 44106-4983. Phone: (216) 368-1856. Fax: (216) 368-4825. E-mail: exp2{at}po.cwru.edu.

Infection and Immunity, September 1998, p. 4425-4430, Vol. 66, No. 9
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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