Hautamaki R D, Kobayashi D K, Senior R M, Shapiro S D
Department of Internal Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, MO 63110, USA.
Science. 1997 Sep 26;277(5334):2002-4. doi: 10.1126/science.277.5334.2002.
To determine which proteinases are responsible for the lung destruction characteristic of pulmonary emphysema, macrophage elastase-deficient (MME-/-) mice were subjected to cigarette smoke. In contrast to wild-type mice, MME-/- mice did not have increased numbers of macrophages in their lungs and did not develop emphysema in response to long-term exposure to cigarette smoke. Smoke-exposed MME-/- mice that received monthly intratracheal instillations of monocyte chemoattractant protein-1 showed accumulation of alveolar macrophages but did not develop air space enlargement. Thus, macrophage elastase is probably sufficient for the development of emphysema that results from chronic inhalation of cigarette smoke.
为了确定哪些蛋白酶导致了肺气肿特有的肺组织破坏,对巨噬细胞弹性蛋白酶缺陷(MME-/-)小鼠进行香烟烟雾暴露。与野生型小鼠不同,MME-/-小鼠肺部巨噬细胞数量没有增加,并且在长期暴露于香烟烟雾后也没有发生肺气肿。每月经气管内滴注单核细胞趋化蛋白-1的烟雾暴露MME-/-小鼠出现肺泡巨噬细胞积聚,但没有出现气腔扩大。因此,巨噬细胞弹性蛋白酶可能足以导致因长期吸入香烟烟雾而引起的肺气肿。