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Title: Allergen-induced airway inflammation and bronchial responsiveness in wild-type and interleukin-4-deficient mice
Authors: Brusselle, G ×
Kips, Johan
Joos, Gustaaf
Bluethmann, H
Pauwels, R #
Issue Date: 1995
Publisher: Amer lung assoc
Series Title: American Journal of Respiratory Cell and Molecular Biology vol:12 issue:3 pages:254-259
Abstract: T helper 2 (Th2)-like cytokines are thought to play a crucial role in the pathogenesis of airway inflammation in atopic asthma, leading to bronchial hyperresponsiveness. To investigate the role of the principal Th2 cytokine interleukin-4 (IL-4) in asthma, we examined the allergen-induced changes in airway morphology and bronchial responsiveness (BR) in an in vivo mouse model. C57BL/6 mice were actively sensitized to ovalbumin (OVA) and exposed daily to aerosolized OVA or saline (SAL) for 7 days. Twenty-four hours after the last allergen exposure, total and differential counts of bronchoalveolar lavage cells revealed a significant increase of eosinophils and lymphocytes in OVA-exposed immunized mice compared with SAL-exposed animals. In IL-4-deficient (IL-4(-/-)) mice, treated in the same way, there were substantially fewer eosinophils in bronchoalveolar lavage compared with wild-type mice. Allergen exposure of actively sensitized wild-type mice induced a significant increase of BR to carbachol and to serotonin compared with SAL-exposed mice. In contrast, OVA exposure of immunized IL-4(-/-) mice did not augment BR to serotonin compared with SAL-challenged IL-4(-/-) mice. In conclusion, these data indicate that repeated allergen exposure in sensitized mice induces airway inflammation and bronchial hyperresponsiveness, and that IL-4 plays a predominant role in the pathogenesis of both phenomena.
ISSN: 1044-1549
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Academic Centre for Nursing and Midwifery
Psychology Research Units (-)
Department of Public Health miscellaneous
× corresponding author
# (joint) last author

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