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Glutathione Can Protect A549 From Smoke-Induced Inhibition of Collagen Gel Contraction* FREE TO VIEW

Hangjun Wang, MD; T. Umino, MD; Xiang-der Liu, MD; Yun Kui Zhu, MD; M. Patricia Leuschen, PhD; John R. Spurzem, MD; Debra J. Romberger, MD, FCCP; Stephen I. Rennard, MD, FCCP
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*From the Section of Pulmonary and Critical Care Medicine, University of Nebraska Medical Center, Omaha, NB.

Correspondence to: Hangjun Wang, MD, Section of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Nebraska Medical Center, 600 South 42nd St, Omaha, NB 68198-5300

Chest. 2000;117(5_suppl_1):248S-249S. doi:10.1378/chest.117.5_suppl_1.248S
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Abbreviation: HFL = human fetal lung fibroblast

In emphysema, alveolar structures are destroyed. This tissue destruction represents a balance between tissue injury and tissue repair, with the balance tipped toward injury. Cigarette smoke cannot only initiate destructive inflammatory processes in the lung, but may also impair repair responses. The current study was designed to compare the effect of cigarette smoke on lung fibroblasts and A549 cells, a bronchoalveolar carcinoma cell line often used as a model of alveolar epithelial cells. As a model of remodeling associated with repair, contraction of three-dimensional native collagen gels was assessed. Both A549 cells plated on top of collagen gels and human fetal lung fibroblast (HFL-1) cells plated inside gels contracted the collagen gels in a time- and cell density-dependent manner. Control HFL-1 contracted gels to 40.1% of initial size, which A549 contracted gels to 62.8%. Five percent smoke extract markedly inhibited HFL-1 mediated contraction (60.8 ± 2.5%; p <0.05) but had little effect on A549 contraction (63.6 ± 1.3%; p > 0.05). As cigarette smoke is an oxidant stress, we next evaluated if A549 was resistant to the effect of cigarette smoke due to glutathione content. Consistent with this, A549 cells contained significantly more glutathione (3.23 vs 0.88 nmol/106 cells; p < 0.05) than did HFL-1 cells. A549 cells also secreted glutathione into the culture medium. Both A549 culture medium and exogenous glutathione were capable of protecting HFL-1 cells from cigarette smoke inhibition of fibroblast gel contraction. Taken together, these studies suggest that alveolar epithelial cells may be able to participate in repair responses following injury including tissue contraction. Such capabilities may be important in limiting alveolar enlargement characteristic of emphysema. Intracellular antioxidant mechanisms may be important in protecting against adverse effects of cigarette smoke, and epithelial cells antioxidants may protect mesenchymal cells.




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