Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/43967
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Type: Journal article
Title: Strain-dependent resistance to allergen-induced lung pathophysiology in mice correlates with rate of apoptosis of lung-derived eosinophils
Author: Tumes, D.
Cormie, J.
Calvert, M.
Stewart, K.
Nassenstein, C.
Braun, A.
Foster, P.
Dent, L.
Citation: Journal of Leukocyte Biology, 2007; 81(6):1362-1373
Publisher: Federation Amer Soc Exp Biol
Issue Date: 2007
ISSN: 0741-5400
1938-3673
Statement of
Responsibility: 
Damon J. Tumes, James Cormie, Michael G. Calvert, Kalev Stewart, Christina Nassenstein, Armin Braun, Paul S. Foster, and Lindsay A. Dent
Abstract: Although exposed to similar allergic and environmental stimuli, not all humans develop asthma. Similarly, mouse strains vary in the degree of pathophysiology seen following induction of experimental asthma. Three mouse strains (CBA/Ca, BALB/c, and C57BL/6) were used to determine if the extent and duration of inflammation influenced the degree of lung tissue damage in an OVA-induced allergic asthma model. Airways obstruction, leukocyte infiltration, edema, eosinophil accumulation, and degranulation were less severe in wild-type (wt) CBA/Ca mice than wt BALB/c and C57BL/6 mice. F1 hybrids of CBA/Ca mice crossed with BALB/c or C57BL/6 mice had bronchoalveolar lavage leukocyte (BAL) and cell-free protein profiles similar to those of the respective disease-susceptible parental strain. IL-5 transgene expression on each of the three genetic backgrounds accentuated the difference between CBA/Ca and the other two strains. Importantly, even when overexpressing IL-5, CBA/Ca mice did not develop substantial airways obstruction. Eosinophils recovered from the airways of allergic wt and IL-5 transgenic (Tg) CBA/Ca mice entered apoptosis at a faster rate than eosinophils from the other parental strains and F1 hybrids. In contrast, eosinophils harvested from the peritoneal cavities of untreated CBA/Ca IL-5 Tg mice had a relatively low rate of apoptosis in vitro. The CBA/Ca mouse strain is therefore relatively resistant to experimental asthma, and this may be a consequence of a propensity for apoptosis of eosinophils recruited into the allergic lung. Restricting survival of a key effector cell may thus limit pathogenesis in this experimental model and in humans.
Keywords: Lung; Eosinophils; Cells, Cultured; Bronchoalveolar Lavage Fluid; Animals; Animals, Genetically Modified; Mice; Asthma; Ovalbumin; Interleukin-5; Allergens; Apoptosis; Species Specificity; Immunity, Innate
Description: © 2007 by Society for Leukocyte Biology
Provenance: Published online before print March 22, 2007
RMID: 0020070905
DOI: 10.1189/jlb.0106046
Appears in Collections:Molecular and Biomedical Science publications

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