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Eur Respir J 2005; 25:15-22
Copyright ©ERS Journals Ltd 2005

Different lung responses to cigarette smoke in two strains of mice sensitive to oxidants

B. Bartalesi, E. Cavarra, S. Fineschi, M. Lucattelli, B. Lunghi, P. A. Martorana and G. Lungarella

Dipartimento di Fisiopatologia e Medicina Sperimentale, Università di Siena, Siena, Italy

CORRESPONDENCE: G. Lungarella, Dipartimento di Fisiopatologia e Medicina Sperimentale, Università di Siena, Via Aldo Moro n.6, I-53100 Siena, Italy. Fax: 39 0577234019. E-mail: lungarella@unisi.it

Keywords: Bronchial changes, emphysema, expression of cytokines, mouse interstrain variations

Received: June 7, 2004
Accepted August 13, 2004

The development of cigarette smoke-induced pulmonary changes in C57 Bl/6J and DBA/2 mice was investigated. Both strains are sensitive to oxidants and C57Bl/6J mice are moderately deficient in serum alpha1-proteinase inhibitor.

Following chronic exposure to cigarette smoke, patchy emphysema was present in mice of both strains, but developed faster in DBA/2 mice. A positive reaction for mouse neutrophil elastase was seen on the septa of both strains. Additionally, the DBA/2 mice developed a uniform parenchymal dilation that was preceded by the appearance of apoptotic cells in areas with a low signal for vascular endothelial growth factor-receptor 2. Fibrotic areas scattered throughout the parenchyma, coupled with a positive immunohistochemical reaction for transforming growth factor-ß was seen only in DBA/2 mice.

Both DBA/2 and C57Bl/6J strains showed epithelial cell injury and areas of deciliation in their airways. However, the appearance of goblet cell metaplasia was common in C57Bl/6J mice but rare in DBA/2 mice. A positive immunohistochemical reaction for interleukin (IL)-4, IL-13 and MUC5AC was seen only in the airways of C57Bl/6J mice.

Strain characteristics (alpha1-proteinase inhibitor levels, sensitivity to oxidants, and constitutive levels of vascular endothelial growth factor-receptor 2) and phenotypical responses (apoptosis and cytokine distribution) may condition parenchymal and airway changes to cigarette smoke.




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