title: CD23 deficient mice develop allergic airway hyperresponsiveness following sensitization with ovalbumin.
abstract: The low affinity receptor for IgE (CD23) is reported to regulate immune and inflammatory events and as a result, it may have a role in the development of allergic airway inflammation and hyperresponsiveness (AHR). To test this hypothesis CD23-deficient mice were studied following different modes of allergic sensitization. Mice were actively sensitized either intraperitoneally with ovalbumin (OA)/alum or via the airways (10 days exposure to OA aerosol with no adjuvant). Passive sensitization was performed by intravenous injections of OA-specific IgE. Airway responsiveness, serum IgE and IgG levels were assessed together with airway inflammation. Passive sensitization followed by airway challenges resulted in increased OA-specific lgG and IgE in the serum of wild-type mice only, while both the CD23+/+ and CD23-/- groups developed tracheal smooth muscle hyperresponsiveness to electrical field stimulation, indicating that IgE/CD23-mediated immune functions may not be necessary for the development of allergic changes. Active sensitization of both CD23-/- and CD23+/+ mice resulted in increased serum levels of OA-specific IgE and lgG, airway eosinophilia and significant AHR when compared with nonsensitized mice. The genetic deficiency of CD23-/- mice not only failed to prevent but was associated with a significant increase of these responses. These results indicate that CD23 may not be essential for the development of allergen-induced AHR and further, that its presence may have some inhibitory effects on the allergic response.
authors.affiliation: Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado 80206, USA.
authors.forename: A
authors.initials: A
authors.lastname: Haczku
authors.forename: K
authors.initials: K
authors.lastname: Takeda
authors.forename: E
authors.initials: E
authors.lastname: Hamelmann
authors.forename: A
authors.initials: A
authors.lastname: Oshiba
authors.forename: J
authors.initials: J
authors.lastname: Loader
authors.forename: A
authors.initials: A
authors.lastname: Joetham
authors.forename: C
authors.initials: C
authors.lastname: Irvin
authors.forename: H
authors.initials: H
authors.lastname: Kikutani
authors.forename: E W
authors.initials: EW
authors.lastname: Gelfand
mesh_terms: D000485:Allergens; D000818:Animals; D016535:Bronchial Hyperreactivity / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000473:pathology; D006969:Hypersensitivity, Immediate / Q000150:complications* / Q000209:etiology; D007073:Immunoglobulin E / Q000032:analysis; D007074:Immunoglobulin G / Q000032:analysis; D066298:In Vitro Techniques; D008168:Lung / Q000473:pathology; D008213:Lymphocyte Activation; D016210:Methacholine Chloride / Q000494:pharmacology; D051379:Mice; D009119:Muscle Contraction; D010047:Ovalbumin / Q000276:immunology*; D017455:Receptors, IgE / Q000172:deficiency*; D014132:Trachea / Q000503:physiopathology
chemical_list: D000485:Allergens; D007074:Immunoglobulin G; D017455:Receptors, IgE; D016210:Methacholine Chloride; D007073:Immunoglobulin E; D010047:Ovalbumin