Antigen-Induced Airway Hyperresponsiveness, Pulmonary Eosinophilia, and Chemokine Expression in B Cell–Deficient Mice
Autor: | George T. De Sanctis, Andrew D. Luster, James A. MacLean, Alain Sauty, Jeffrey M. Drazen |
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Rok vydání: | 1999 |
Předmět: |
Pulmonary and Respiratory Medicine
Eotaxin Chemokine Pathology medicine.medical_specialty Ovalbumin Clinical Biochemistry Mice Antibody Specificity Respiratory Hypersensitivity medicine Animals RNA Messenger Pulmonary Eosinophilia Lung Molecular Biology B cell B-Lymphocytes biology business.industry Monocyte Interleukin Cell Biology Immunoglobulin E respiratory system Eosinophil Asthma Mice Mutant Strains respiratory tract diseases medicine.anatomical_structure Immunology biology.protein Chemokines business Bronchoalveolar Lavage Fluid |
Zdroj: | American Journal of Respiratory Cell and Molecular Biology. 20:379-387 |
ISSN: | 1535-4989 1044-1549 |
DOI: | 10.1165/ajrcmb.20.3.3291 |
Popis: | 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. |
Databáze: | OpenAIRE |
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