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Am. J. Respir. Cell Mol. Biol., Volume 20, Number 3, March, 1999 379-387

Antigen-Induced Airway Hyperresponsiveness, Pulmonary Eosinophilia, and Chemokine Expression in B Cell-Deficient Mice

James A. MacLean, Alain Sauty, Andrew D. Luster, Jeffrey M. Drazen, and George T. De Sanctis

Clinical Immunology and Allergy Unit and Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital; Partners Asthma Center; and Harvard Medical School, Boston, Massachusetts

Murine models of allergen-induced pulmonary inflammation share many features with human asthma, including the development of antigen-induced pulmonary eosinophilia, airway hyperresponsiveness, antigen-specific cellular and antibody responses, the elaboration of Th2 cytokines (interleukin [IL]-4 and IL-5), and the expression of chemokines with activity for eosinophils. We examined the role of B cells and antigen-specific antibody responses in such a model by studying the histopathologic and physiologic responses of B cell-deficient mice compared with wild-type controls, following systemic immunization and airway challenge with ovalbumin (OVA). Both OVA-challenged wild-type and B cell-deficient mice developed (1) airway hyperresponsiveness, (2) pulmonary inflammation with activated T cells and eosinophils, (3) IL-4 and IL-5 secretion into the airway lumen, and (4) increased expression of the eosinophil active chemokines eotaxin and monocyte chemotactic protein-3. There were no significant differences in either the pathologic or physiologic responses in the B cell-deficient mice compared with wild-type mice. These data indicate that B cells and antigen-specific antibodies are not required for the development of airway hyperresponsiveness, eosinophilic pulmonary inflammation, and chemokine expression in sensitized mice following aerosol challenge with antigen.




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