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

B Bartalesi, E Cavarra, S Fineschi… - European …, 2005 - Eur Respiratory Soc
B Bartalesi, E Cavarra, S Fineschi, M Lucattelli, B Lunghi, PA Martorana, G Lungarella
European Respiratory Journal, 2005Eur Respiratory Soc
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 …
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-β 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.
European Respiratory Society