Faculty Research 1990 - 1999

Development of eosinophilic airway inflammation and airway hyperresponsiveness in mast cell-deficient mice.

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Animal, Bronchial-Hyperreactivity: pp, pa, Bronchoalveolar-Lavage-Fluid: im, Eosinophils: pa, Female, IgE: bi, IgG: bi, Lung: im, pa, Lung-Compliance: im, Mast-Cells: im, pa, Mice, Mice-Inbred-C57BL, Mice-Mutant-Strains, Ovalbumin: im, SUPPORT-U-S-GOVT-P-H-S

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JAX Source

J Exp Med 1997 Aug 4;186(3):449-54


HL36577/HL/NHLBI, CA20408/CA/NCI


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.