Mast cells are the main effector cells of immediate hypersensitivity and anaphylaxis. Their role in the development of allergen-induced airway hyperresponsiveness (AHR) is controversial and based on indirect evidence. To address these issues, mast cell–deficient mice (W/W v) and their congenic littermates were sensitized to ovalbumin (OVA) by intraperitoneal injection and subsequently challenged with OVA via the airways. Comparison of OVA-specific immunoglobulin E (IgE) levels in the serum and numbers of eosinophils in bronchoalveolar lavage fluid or lung digests showed no differences between the two groups of mice. Further, measurements of airway resistance and dynamic compliance at baseline and after inhalation of methacholine were similar. These data indicate that mast cells or IgE–mast cell activation is not required for the development of eosinophilic inflammation and AHR in mice sensitized to allergen via the intraperitoneal route and challenged via the airways.
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4 August 1997
Brief Definitive Report|
August 04 1997
Development of Eosinophilic Airway Inflammation and Airway Hyperresponsiveness in Mast Cell–deficient Mice
K. Takeda,
K. Takeda
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
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E. Hamelmann,
E. Hamelmann
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
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A. Joetham,
A. Joetham
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
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L.D. Shultz,
L.D. Shultz
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
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G.L. Larsen,
G.L. Larsen
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
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C.G. Irvin,
C.G. Irvin
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
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E.W. Gelfand
E.W. Gelfand
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
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K. Takeda
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
E. Hamelmann
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
A. Joetham
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
L.D. Shultz
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
G.L. Larsen
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
C.G. Irvin
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
E.W. Gelfand
From the *Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, and the ‡Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and §The Jackson Laboratory, Bar Harbor, Maine
Address correspondence to Dr. Erwin Gelfand, Department of Pediatrics, Room K801, University of Colorado Health Sciences Center, 1400 Jackson Street, Denver, CO 80206. Phone: 303-398-1196; FAX: 303-270-2105; E-mail: [email protected]
The assistance of Ms. D. Nabighian in preparation of this manuscript is gratefully acknowledged.
Received:
April 11 1997
Revision Received:
May 30 1997
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1997
J Exp Med (1997) 186 (3): 449–454.
Article history
Received:
April 11 1997
Revision Received:
May 30 1997
Citation
K. Takeda, E. Hamelmann, A. Joetham, L.D. Shultz, G.L. Larsen, C.G. Irvin, E.W. Gelfand; Development of Eosinophilic Airway Inflammation and Airway Hyperresponsiveness in Mast Cell–deficient Mice . J Exp Med 4 August 1997; 186 (3): 449–454. doi: https://doi.org/10.1084/jem.186.3.449
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