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Am J Physiol Lung Cell Mol Physiol (March 7, 2003). doi:10.1152/ajplung.00390.2002
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Submitted on November 18, 2002
Accepted on March 2, 2003

Allergen Induced Airway Disease is Mouse Strain Dependent

Gregory S. Whitehead1*, Julia K.L. Walker1, Katherine G. Berman1, W. Michael Foster1, and David A. Schwartz2

1 Department of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, NC, USA
2 Department of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, NC, USA; VA Medical Center, Durham, NC, USA

* To whom correspondence should be addressed. E-mail: white141{at}mc.duke.edu.

We investigated the development of airway hyperreactivity (AHR) and inflammation in the lungs of 9 genetically diverse inbred strains of mice (129/SvIm, A/J, BALB/cJ, BTBR+(T)/tf/tf, CAST/Ei, C3H/HeJ, C57BL/6J, DBA/2J, and FVB/NJ) following sensitization and challenge with ovalbumin (OVA). At 24, 48, and 72 hours post OVA exposure, the severity of AHR and eosinophilic inflammation of the mouse strains ranged from relatively unresponsive to responsive. The severity of the airway eosinophilia of some strains did not clearly correlate with the development of AHR. The temporal presence of Th-2 cytokines in lung lavage fluid also varied markedly among the strains. The levels of IL-4 and IL-13 were generally increased in the strains with the highest airway eosinophilia at 24 and 72 hours post-exposure, respectively; and the levels of IL-5 were significantly increased in most of the strains with airway inflammation over the 72-hour time period. The differences of physiologic and biological responses among the inbred mouse strains after OVA sensitization and challenge support the hypothesis that genetic factors contribute, in part, to the development of allergen-induced airway disease.




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