Expression of fas (CD95) and fast (CD95L) in human airway epithelium

被引:72
作者
Hamann, KJ
Dorscheid, DR
Ko, FD
Conforti, AE
Sperling, AI
Rabe, KF
White, SR
机构
[1] Univ Chicago, Pulm & Crit Care Med Sect, Div Biol Sci, Chicago, IL 60637 USA
[2] Krankenhaus Grosshansdorf, D-2070 Grosshansdorf, Germany
关键词
D O I
10.1165/ajrcmb.19.4.3100
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
The cell surface molecule Fas (CD95) is a member of the tumor necrosis factor receptor family. Ligation of the Fas receptor can lead to induction of apoptosis in inflammatory cells. It has been suggested that expression of the Fas receptor and its ligand (FasL) in airway epithelium may modulate the inflammatory response commonly found in asthmatic lungs. We examined Fas and Fast expression on primary human tissues, on bronchial epithelial cells in primary culture, and on the immortalized human airway epithelial cell line, 1HAE(o)(-). Receptor and ligand expression were demonstrated using multiple antibodies and multiple techniques, including immunohistochemistry, flow cytometry, Western blots, and reverse transcription-polymerase chain reaction (RT-PCR). Immunohistochemical staining demonstrated that both columnar and basal cells of intact human lung tissues expressed cell surface Fas and Fast. In addition, both primary cultured and immortalized 1HAE(o)(-) cells expressed cell surface Fas and Fast, as demonstrated by flow cytometry; expression of Fas and Fast was confirmed at the transcription level using RT-PCR and, for additional confirmation of Fast, using Western blots. We demonstrate that both Fas and Fast are expressed by human airway epithelial cell subtypes. Expression of these molecules may play an important role in regulation of the inflammatory response.
引用
收藏
页码:537 / 542
页数:6
相关论文
共 29 条
[1]  
Bellairs P, 1995, AUSTRALAS I MIN MET, V95, P63
[2]  
Cohen Philip L., 1995, P169
[3]   CFTR EXPRESSION AND CHLORIDE SECRETION IN POLARIZED IMMORTAL HUMAN BRONCHIAL EPITHELIAL-CELLS [J].
COZENS, AL ;
YEZZI, MJ ;
KUNZELMANN, K ;
OHRUI, T ;
CHIN, L ;
ENG, K ;
FINKBEINER, WE ;
WIDDICOMBE, JH ;
GRUENERT, DC .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1994, 10 (01) :38-47
[4]   CELL-PROLIFERATION IN THE BRONCHIAL-MUCOSA OF ASTHMATICS AND CHRONIC BRONCHITICS [J].
DEMOLY, P ;
SIMONYLAFONTAINE, J ;
CHANEZ, P ;
PUJOL, JL ;
LEQUEUX, N ;
MICHEL, FB ;
BOUSQUET, J .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 150 (01) :214-217
[5]   Fas-mediated apoptosis in cultured human eosinophils [J].
Druilhe, A ;
Cai, ZZ ;
Haile, S ;
Chouaib, S ;
Pretolani, M .
BLOOD, 1996, 87 (07) :2822-2830
[6]  
French L E, 1996, Behring Inst Mitt, P156
[7]   Fas and Fas ligand in embryos and adult mice: Ligand expression in several immune-privileged tissues and coexpression in adult tissues characterized by apoptotic cell turnover [J].
French, LE ;
Hahne, M ;
Viard, I ;
Radlgruber, G ;
Zanone, R ;
Becker, K ;
Muller, C ;
Tschopp, J .
JOURNAL OF CELL BIOLOGY, 1996, 133 (02) :335-343
[8]   Potential involvement of fas and its ligand in the pathogenesis of Hashimoto's thyroiditis [J].
Giordano, C ;
Stassi, G ;
DeMaria, R ;
Todaro, M ;
Richiusa, P ;
Papoff, G ;
Ruberti, G ;
Bagnasco, M ;
Testi, R ;
Galluzzo, A .
SCIENCE, 1997, 275 (5302) :960-963
[9]   CULTURE AND TRANSFORMATION OF HUMAN AIRWAY EPITHELIAL-CELLS [J].
GRUENERT, DC ;
FINKBEINER, WE ;
WIDDICOMBE, JH .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1995, 268 (03) :L347-L360
[10]   Expression and function of the Fas receptor on human blood and tissue eosinophils [J].
Hebestreit, H ;
Yousefi, S ;
Balatti, I ;
Weber, M ;
Crameri, R ;
Simon, D ;
Hartung, K ;
Schapowal, A ;
Blaser, K ;
Simon, HU .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1996, 26 (08) :1775-1780