Cigarette smoke inhibits human bronchial epithelial cell repair processes

被引:117
作者
Wang, HJ
Liu, XD
Umino, T
Sköld, CM
Zhu, YK
Kohyama, T
Spurzem, JR
Romberger, DJ
Rennard, SI
机构
[1] Univ Nebraska, Med Ctr, Omaha, NE 68198 USA
[2] Mt Sinai Hosp, Toronto, ON M5G 1X5, Canada
[3] Tokyo Med & Dent Univ, Tokyo, Japan
[4] Karolinska Inst, Stockholm, Sweden
关键词
D O I
10.1165/ajrcmb.25.6.4458
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
By interfering with the ability of airway epithelial cells to support repair processes, cigarette smoke could contribute to alterations of airway structures and functions that characterize chronic obstructive pulmonary disease (COPD). The current study assessed the ability of cigarette smoke extract (CSE) to alter human airway epithelial cell chemotaxis, proliferation, and contraction of three-dimensional collagen gels, a model of extracellular matrix remodeling. The volatile components contained in cigarette smoke, acetaldehyde and acrolein, were able to inhibit all three processes. Nonvolatile components contained within lyophilized CSE also inhibited chemotaxis but displayed no activity in the other two bioassays. CSE also inhibited the ability of airway epithelial cells to release transforming growth factor (TGF)-beta and fibronectin. Exogenous fibronectin was unable to restore epithelial cell contraction of collagen gels. Exogenous TGF-beta partially restored the ability of airway epithelial cells to contract collagen gels and to produce fibronectin. This supports a role for inhibition of TGF-beta release in mediating the inhibitory effects of cigarette smoke. Taken together, the results of the current study suggest that epithelial cells present in the airways of smokers may be altered in their ability to support repair responses, which may contribute to architectural disruptions present in the airways in COPD associated with cigarette smoking.
引用
收藏
页码:772 / 779
页数:8
相关论文
共 30 条
[1]   COLLAGEN GEL CONTRACTION BY FIBROBLASTS REQUIRES CELLULAR FIBRONECTIN BUT NOT PLASMA FIBRONECTIN [J].
ASAGA, H ;
KIKUCHI, S ;
YOSHIZATO, K .
EXPERIMENTAL CELL RESEARCH, 1991, 193 (01) :167-174
[2]  
BARROW RE, 1992, LUNG, V170, P331
[3]   SERUM-FREE CULTURE OF FRACTIONATED BOVINE BRONCHIAL EPITHELIAL-CELLS [J].
BECKMANN, JD ;
TAKIZAWA, H ;
ROMBERGER, D ;
ILLIG, M ;
CLAASSEN, L ;
RICKARD, K ;
RENNARD, SI .
IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL, 1992, 28A (01) :39-46
[4]   PRODUCTION OF A TISSUE-LIKE STRUCTURE BY CONTRACTION OF COLLAGEN LATTICES BY HUMAN-FIBROBLASTS OF DIFFERENT PROLIFERATIVE POTENTIAL INVITRO [J].
BELL, E ;
IVARSSON, B ;
MERRILL, C .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1979, 76 (03) :1274-1278
[5]  
BUIST AS, 1994, TXB RESP MED, P1259
[6]   EFFECTS OF CIGARETTE-SMOKE EXTRACT ON BOVINE BRONCHIAL EPITHELIAL-CELL ATTACHMENT AND MIGRATION [J].
CANTRAL, DE ;
SISSON, JH ;
VEYS, T ;
RENNARD, SI ;
SPURZEM, JR .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1995, 268 (05) :L723-L728
[7]   Cigarette smoke extract inhibits fibroblast-mediated collagen gel contraction [J].
Carnevali, S ;
Nakamura, Y ;
Mio, T ;
Liu, X ;
Takigawa, K ;
Romberger, DJ ;
Spurzem, JR ;
Rennard, SI .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1998, 274 (04) :L591-L598
[8]  
CARP H, 1978, AM REV RESPIR DIS, V118, P617
[9]   Effect of aprotinin on smooth muscle cell proliferation, migration, and extracellular matrix synthesis [J].
Horodyski, J ;
Powell, RJ .
JOURNAL OF SURGICAL RESEARCH, 1996, 66 (02) :115-118
[10]   DETERMINATION OF FORMALDEHYDE AND ACETALDEHYDE IN MAINSTREAM CIGARETTE-SMOKE BY HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY [J].
HOULGATE, PR ;
DHINGRA, KS ;
NASH, SJ ;
EVANS, WH .
ANALYST, 1989, 114 (03) :355-360