CD23 deficient mice develop allergic airway hyperresponsiveness following sensitization with ovalbumin

Angela Franciska Haczku, Katsuyuki Takeda, Eckard Hamelmann, Akihiro Oshiba, Joan Loader, Anthony Joetham, Charles Irvin, Hitoshi Kikutani, Erwin W. Gelfand

Research output: Contribution to journalArticle

50 Citations (Scopus)

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 IgG 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 IgG, 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.

Original languageEnglish (US)
Pages (from-to)1945-1955
Number of pages11
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume156
Issue number6
StatePublished - 1997
Externally publishedYes

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Ovalbumin
Immunoglobulin E
Immunoglobulin G
Serum
Inflammation
IgE Receptors
Eosinophilia
Aerosols
Intravenous Injections
Allergens
Electric Stimulation
Smooth Muscle

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Haczku, A. F., Takeda, K., Hamelmann, E., Oshiba, A., Loader, J., Joetham, A., ... Gelfand, E. W. (1997). CD23 deficient mice develop allergic airway hyperresponsiveness following sensitization with ovalbumin. American Journal of Respiratory and Critical Care Medicine, 156(6), 1945-1955.

CD23 deficient mice develop allergic airway hyperresponsiveness following sensitization with ovalbumin. / Haczku, Angela Franciska; Takeda, Katsuyuki; Hamelmann, Eckard; Oshiba, Akihiro; Loader, Joan; Joetham, Anthony; Irvin, Charles; Kikutani, Hitoshi; Gelfand, Erwin W.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 156, No. 6, 1997, p. 1945-1955.

Research output: Contribution to journalArticle

Haczku, AF, Takeda, K, Hamelmann, E, Oshiba, A, Loader, J, Joetham, A, Irvin, C, Kikutani, H & Gelfand, EW 1997, 'CD23 deficient mice develop allergic airway hyperresponsiveness following sensitization with ovalbumin', American Journal of Respiratory and Critical Care Medicine, vol. 156, no. 6, pp. 1945-1955.
Haczku, Angela Franciska ; Takeda, Katsuyuki ; Hamelmann, Eckard ; Oshiba, Akihiro ; Loader, Joan ; Joetham, Anthony ; Irvin, Charles ; Kikutani, Hitoshi ; Gelfand, Erwin W. / CD23 deficient mice develop allergic airway hyperresponsiveness following sensitization with ovalbumin. In: American Journal of Respiratory and Critical Care Medicine. 1997 ; Vol. 156, No. 6. pp. 1945-1955.
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