Different lung responses to cigarette smoke in two strains of mice sensitive to oxidants
Different lung responses to cigarette smoke in two strains of mice sensitive to oxidants
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DOI：
10.1183/09031936.04.00067204
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发表时间：
2005-01-01
影响因子：
24.3
通讯作者：
Lungarella, G
中科院分区：
文献类型：
--
作者：
Bartalesi, B;Cavarra, E;Lungarella, G
研究了 C57 Bl/6J 和 DBA/2 小鼠中香烟烟雾引起的肺部变化的发展。两种品系均对氧化剂敏感，并且C57Bl/6J小鼠血清α-蛋白酶抑制剂中度缺乏。长期接触香烟烟雾后，两种品系的小鼠均出现斑片状肺气肿，但DBA/2小鼠发展更快。在两种菌株的隔膜上都观察到小鼠中性粒细胞弹性蛋白酶的阳性反应。此外，DBA/2 小鼠出现均匀的实质扩张，随后在血管内皮生长因子受体 2 信号低的区域出现凋亡细胞。仅在 DBA/2 小鼠中观察到分散在整个实质中的纤维化区域，以及转化生长因子-β 的阳性免疫组织化学反应。DBA/2 和 C57Bl/6J 品系均显示上皮细胞损伤和他们的呼吸道退化。然而，杯状细胞化生的出现在C57Bl/6J小鼠中很常见，但在DBA/2小鼠中很少见。仅在 C57Bl/6J 小鼠的气道中观察到白细胞介素 (IL)-4、IL-13 和 MUC5AC 的阳性免疫组织化学反应。品系特征（α-蛋白酶抑制剂水平、对氧化剂的敏感性和血管内皮生长因子受体 2 的组成水平）和表型反应（细胞凋亡和细胞因子分布）可能会影响实质和气道对香烟烟雾的变化。
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 alphal-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-beta 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 (alphal-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.