TRAIL and its receptors in the colonic epithelium:: A putative role in the defense of viral infections

被引:79
作者
Sträter, J
Walczak, H
Pukrop, T
Von Müller, L
Hasel, C
Kornmann, M
Mertens, T
Möller, P
机构
[1] Univ Ulm, Dept Pathol, D-89081 Ulm, Germany
[2] Univ Ulm, Dept Virol, D-89081 Ulm, Germany
[3] Univ Ulm, Dept Surg, D-89081 Ulm, Germany
[4] Deutsch Krebsforschungszentrum, D-6900 Heidelberg, Germany
关键词
D O I
10.1053/gast.2002.31889
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor family and induces apoptosis by cross-linking either of the 2 TRAIL receptors containing a death domain (TRAIL-R1 or TRAIL-R2). TRAIL-R3 and TRAIL-R4 are receptors that do not transmit an apoptotic signal. The aim of this study was to investigate the expression and function of TRAIL and its receptors in normal colonic epithelium. Methods: TRAIL and TRAIL receptor expression was studied by reverse-transcriptase polymerase chain reaction and immunohistochemistry. TRAIL sensitivity of epithelial cells was determined in vitro. Results: Normal colonic epithelial cells express TRAIL, TRAIL-R1, TRAIL-R2, and TRAIL-R4. Interestingly, TRAIL and TRAIL-R2 are coexpressed mostly in the luminal surface epithelium. Despite the expression of apoptosis-mediating TRAIL receptors, the normal colonic crypt epithelium is completely resistant to TRAIL-induced apoptosis in vitro. Using an infection model with restricted human cytomegalovirus gene expression or productive adenovirus infection in the colon carcinoma cell line Caco-2, we show that TRAIL sensitivity of colonic epithelial cells is induced on virus infection along with an up-regulation of TRAIL-R1 and TRAIL-R2 on the cell surface. Conclusions: We conclude that the TRAIL system may play a role in the early elimination of virus-infected epithelial cells in the normal gut.
引用
收藏
页码:659 / 666
页数:8
相关论文
共 30 条
[1]   The novel receptor TRAIL-R4 induces NF-κB and protects against TRAIL-mediated apoptosis, yet retains an incomplete death domain [J].
Degli-Esposti, MA ;
Dougall, WC ;
Smolak, PJ ;
Waugh, JY ;
Smith, CA ;
Goodwin, RG .
IMMUNITY, 1997, 7 (06) :813-820
[2]   Cloning and characterization of TRAIL-R3, a novel member of the emerging TRAIL receptor family [J].
DegliEsposti, MA ;
Smolak, PJ ;
Walczak, H ;
Waugh, J ;
Huang, CP ;
DuBose, RF ;
Goodwin, RG ;
Smith, CA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (07) :1165-1170
[3]   Interleukin-18 protects mice against acute herpes simplex virus type 1 infection [J].
Fujioka, N ;
Akazawa, R ;
Ohashi, K ;
Fujii, M ;
Ikeda, M ;
Kurimoto, M .
JOURNAL OF VIROLOGY, 1999, 73 (03) :2401-2409
[4]  
García VE, 1999, J IMMUNOL, V162, P6114
[5]   Monocyte-mediated tumoricidal activity via the tumor necrosis factor-related cytokine, TRAIL [J].
Griffith, TS ;
Wiley, SR ;
Kubin, MZ ;
Sedger, LM ;
Maliszewski, CR ;
Fanger, NA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (08) :1343-1353
[6]  
HALL PA, 1994, J CELL SCI, V107, P3569
[7]  
Hauri H P, 1991, Semin Cell Biol, V2, P355
[8]  
Kayagaki N, 1999, J IMMUNOL, V162, P2639
[9]  
Mariani SM, 1998, EUR J IMMUNOL, V28, P973, DOI 10.1002/(SICI)1521-4141(199803)28:03<973::AID-IMMU973>3.3.CO
[10]  
2-K