Department of Pulmonary Medicine, Hospital Clínic-Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Barcelona, Spain.
COPD. 2012 Aug;9(5):473-84. doi: 10.3109/15412555.2012.691999. Epub 2012 Jun 18.
Cigarette smoke (CS) induces an inflammatory process in the lung that may underlie the development of chronic obstructive pulmonary disease (COPD). The nature and characteristics of this process have not been fully established in animal models. We aimed to evaluate the pulmonary inflammatory reaction and its involvement in structural changes in guinea pigs chronically exposed to CS. 19 Hartley guinea pigs were exposed to 7 cigarettes/day, during 3 or 6 months. 18 control guinea pigs were sham-exposed. Numbers of neutrophils, macrophages and eosinophils and lymphoid follicles were assessed in different lung structures. Airway and vessel morphometry, alveolar space size and collagen deposition were also quantified. After 6 months of exposure, CS-exposed guinea pigs showed increased numbers of neutrophils, macrophages and eosinophils in the airways, intrapulmonary vessels and alveolar septa, as well as lymphoid follicles. Increased numbers of muscularized intrapulmonary vessels were apparent at 3 months. After 6 months of exposure, the airway wall thickened and the alveolar space size increased. Collagen deposition was also apparent in airway walls and alveolar septa after 6 months' exposure. The magnitude of airway wall-thickening correlated with the number of infiltrating inflammatory cells, and the extension of collagen deposition correlated with alveolar space size. We conclude that in the guinea pig, 6 months of CS exposure induces inflammatory cell infiltrate in lung structures, at an intensity that correlates with airway remodelling. These changes resemble those observed in COPD, thus endorsing the pathogenic role of CS and the usefulness of this animal model for its study.
香烟烟雾（CS）会在肺部引发炎症反应，这可能是慢性阻塞性肺疾病（COPD）发展的基础。在动物模型中，尚未完全确定这一过程的性质和特征。我们旨在评估慢性 CS 暴露的豚鼠肺部炎症反应及其在结构变化中的作用。19 只 Hartley 豚鼠每天暴露于 7 支香烟中，持续 3 或 6 个月。18 只对照豚鼠进行假暴露。评估了不同肺结构中的中性粒细胞、巨噬细胞和嗜酸性粒细胞以及淋巴滤泡的数量。还定量了气道和血管形态、肺泡腔大小和胶原沉积。暴露 6 个月后，CS 暴露的豚鼠在气道、肺内血管和肺泡隔以及淋巴滤泡中显示出中性粒细胞、巨噬细胞和嗜酸性粒细胞数量增加。3 个月时，可见肌化的肺内血管数量增加。暴露 6 个月后，气道壁变厚，肺泡腔大小增加。气道壁和肺泡隔也出现胶原沉积。气道壁增厚的程度与浸润性炎症细胞的数量相关，胶原沉积的扩展与肺泡腔大小相关。我们得出结论，在豚鼠中，6 个月的 CS 暴露会在肺部结构中引起炎症细胞浸润，其强度与气道重塑相关。这些变化类似于 COPD 中观察到的变化，从而支持 CS 的致病作用和该动物模型在其研究中的有用性。
