Selman M, Montaño M, Ramos C, Vanda B, Becerril C, Delgado J, Sansores R, Barrios R, Pardo A
Instituto Nacional de Enfermedades Respiratorias, Tlalpan Mexico DF.
Am J Physiol. 1996 Nov;271(5 Pt 1):L734-43. doi: 10.1152/ajplung.1996.271.5.L734.
We examined the expression of interstitial collagenase and its enzymatic activity in lung damage induced by tobacco smoke. Guinea pigs were exposed to the smoke of 20 cigarettes per day from 1-8 wk. Age-matched guinea pigs were used as controls. At 6 and 8 wk of smoke exposure, lungs exhibited interstitial and peribronchiolar inflammation and moderate emphysematous changes. In situ hybridization of injured lungs revealed patchy expression of collagenase mRNA mainly in macrophages but also in alveolar epithelial and interstitial cells. Immunoreactive protein was detected in alveolar macrophages and in the alveolar walls and interstitium. Collagenolytic activity increased beginning in the 4th wk of exposure (0.7 +/- 0.43 micrograms collagen degraded/mg collagen incubated relative to 0.23 +/- 0.14 in controls; P < 0.05). At 6 and 8 wk, values were 0.85 +/- 0.34 and 0.98 +/- 0.33 compared with 0.25 +/- 0.11 and 0.26 +/- 13 in controls (P < 0.005 and 0.001). Collagen concentration decreased from 50.7 +/- 8.5 mg/g dry wt in control lungs to 40.2 +/- 5.0 and 42.9 +/- 6.0 at 6 and 8 wk of exposure, respectively (P < 0.05). These results strongly suggest that increased interstitial collagen degradation plays a role in the development of lung emphysema.
我们研究了间质胶原酶在烟草烟雾诱导的肺损伤中的表达及其酶活性。将豚鼠从第1至8周每天暴露于20支香烟的烟雾中。以年龄匹配的豚鼠作为对照。在烟雾暴露6周和8周时，肺呈现间质和细支气管周围炎症以及中度肺气肿改变。对受损肺进行原位杂交显示，胶原酶mRNA呈片状表达，主要在巨噬细胞中，但也存在于肺泡上皮细胞和间质细胞中。在肺泡巨噬细胞以及肺泡壁和间质中检测到免疫反应性蛋白。胶原酶活性从暴露第4周开始增加（相对于对照组的0.23±0.14，每毫克孵育胶原降解0.7±0.43微克胶原；P<0.05）。在6周和8周时，与对照组的0.25±0.11和0.26±0.13相比，数值分别为0.85±0.34和0.98±0.33（P<0.005和0.001）。胶原浓度从对照肺中的50.7±8.5毫克/克干重分别降至暴露6周和8周时的40.2±5.0和42.9±6.0（P<0.05）。这些结果有力地表明，间质胶原降解增加在肺气肿的发展中起作用。
