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Am. J. Respir. Crit. Care Med., Vol 155, No. 3, Mar 1997, 819-825.

Antiinterleukin-5 antibody prevents airway hyperresponsiveness in a murine model of airway sensitization

E Hamelmann, A Oshiba, J Loader, GL Larsen, G Gleich, J Lee and EW Gelfand
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206, USA.

Eosinophils play a central role in the inflammatory response associated with bronchial asthma. We studied the involvement of eosinophils in the development of airway hyperresponsiveness (AHR) in a mouse model of allergic airway sensitization. Sensitization of BALB/c mice to OVA via the airways induced allergen-specific T-cell responses, IgE production, immediate cutaneous hypersensitivity (ICH), and increased airway reactivity. Airway sensitization was associated with eosinophil infiltration of the airways and increased production of interleukin-5 (IL-5) in cultures of peribronchial lymph node cells. Treatment of OVA- challenged animals with anti-IL-5 antibody during the sensitization protocol completely abolished the infiltration of eosinophils into the lung tissue and prevented the development of AHR without affecting levels of allergen-specific IgE, cutaneous hypersensitivity and allergen-specific T cell responses. These findings demonstrate that infiltration of lung tissue by eosinophils, triggered by increased IL-5 production, is a major factor in the development of AHR in this mouse model of airway sensitization.


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[Abstract] [Full Text] [PDF]


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J. Pharmacol. Exp. Ther.Home page
P. Zia-Amirhosseini, E. Minthorn, L. J. Benincosa, T. K. Hart, C. S. Hottenstein, L. A. P. Tobia, and C. B. Davis
Pharmacokinetics and Pharmacodynamics of SB-240563, a Humanized Monoclonal Antibody Directed to Human Interleukin-5, in Monkeys
J. Pharmacol. Exp. Ther., December 1, 1999; 291(3): 1060 - 1067.
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J. Immunol.Home page
J. Schwarze, M. Makela, G. Cieslewicz, A. Dakhama, M. Lahn, T. Ikemura, A. Joetham, and E. W. Gelfand
Transfer of the Enhancing Effect of Respiratory Syncytial Virus Infection on Subsequent Allergic Airway Sensitization by T Lymphocytes
J. Immunol., November 15, 1999; 163(10): 5729 - 5734.
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Am. J. Respir. Cell Mol. Bio.Home page
E. Hamelmann, K. Takeda, J. Schwarze, A. T. Vella, C. G. Irvin, and E. W. Gelfand
Development of Eosinophilic Airway Inflammation and Airway Hyperresponsiveness Requires Interleukin-5 but Not Immunoglobulin E or B Lymphocytes
Am. J. Respir. Cell Mol. Biol., October 1, 1999; 21(4): 480 - 489.
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Am. J. Respir. Crit. Care Med.Home page
A. TOMKINSON, A. KANEHIRO, N. RABINOVITCH, A. JOETHAM, G. CIESLEWICZ, and E. W. GELFAND
The Failure of STAT6-deficient Mice to Develop Airway Eosinophilia and Airway Hyperresponsiveness Is Overcome by Interleukin-5
Am. J. Respir. Crit. Care Med., October 1, 1999; 160(4): 1283 - 1291.
[Abstract] [Full Text]