TNFα production to TLR2 ligands in active IBD patients

被引:54
作者
Cantó, E
Ricart, E
Monfort, D
González-Juan, D
Balanzó, J
Rodríguez-Sánchez, JL
Vidal, S [1 ]
机构
[1] Hosp Santa Creu & Sant Pau, Dept Immunol, Barcelona, Spain
[2] Inst Recerca, Barcelona, Spain
[3] Hosp Santa Creu & Sant Pau, Dept Gastroenterol, Barcelona, Spain
关键词
Crohn's disease; ulcerative colitis; TNF alpha; TLR;
D O I
10.1016/j.clim.2005.12.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Strong evidence suggests that microbial components are involved in the etiopathology of inflammatory bowel diseases (IBD). Since pathogen-associated molecular patterns are recognized by TLRs, dysregutation of TLR-mediated microbial recognition could be taking place in IBD patients. An in vitro assay with different TLR agonists was used to reproduce the immunostimulation via TLR ligands. Elevated TNF alpha production was found in response to LTA and Zymosan in 48% of active Crohn's disease and ulcerative colitis patients when compared to inactive patients or controls. The expression of CD14 did not differ in active patients, whereas TLR2 was significantly upregulated on monocytes from 71% of those patients with high production of TNF alpha. The marked increase of TNF alpha response to TLR2 ligands correlated with a higher TLR2 expression in a group of IBD patients, suggesting that an abnormal mechanism may provide an excess of inflammatory mediators during the active phase of IBDs. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:156 / 165
页数:10
相关论文
共 42 条
[1]   Decreased expression of toll-like receptor-4 and MD-2 correlates with intestinal epithelial cell protection against dysregulated proinflammatory gene expression in response to bacterial lipopolysaccharide [J].
Abreu, MT ;
Vora, P ;
Faure, E ;
Thomas, LS ;
Arnold, ET ;
Arditi, M .
JOURNAL OF IMMUNOLOGY, 2001, 167 (03) :1609-1616
[2]   Toll-like receptor signalling [J].
Akira, S ;
Takeda, K .
NATURE REVIEWS IMMUNOLOGY, 2004, 4 (07) :499-511
[3]   The proinflammatory CD14+CD16+DR++ monocytes are a major source of TNF [J].
Belge, KU ;
Dayyani, F ;
Horelt, A ;
Siedlar, M ;
Frankenberger, M ;
Frankenberger, B ;
Espevik, T ;
Ziegler-Heitbrock, L .
JOURNAL OF IMMUNOLOGY, 2002, 168 (07) :3536-3542
[4]  
BEST WR, 1976, GASTROENTEROLOGY, V70, P439
[5]   Differential alteration in intestinal epithelial cell expression of Toll-like receptor 3 (TLR3) and TLR4 in inflammatory bowel disease [J].
Cario, E ;
Podolsky, DK .
INFECTION AND IMMUNITY, 2000, 68 (12) :7010-7017
[6]   Increased serum levels of eotaxin in patients with inflammatory bowel disease [J].
Chen, W ;
Paulus, B ;
Shu, D ;
Wilson, I ;
Chadwick, V .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 2001, 36 (05) :515-520
[7]   A subset of human dendritic cells in the T cell area of mucosa-associated lymphoid tissue with a high potential to produce TNF-α [J].
de Baey, A ;
Mende, I ;
Baretton, G ;
Greiner, A ;
Hartl, WH ;
Baeuerle, PA ;
Diepolder, HM .
JOURNAL OF IMMUNOLOGY, 2003, 170 (10) :5089-5094
[8]   TUMOR-NECROSIS-FACTOR ANTIBODY TREATMENT IN CROHNS-DISEASE [J].
DERKX, B ;
TAMINIAU, J ;
RADEMA, S ;
STRONKHORST, A ;
WORTEL, C ;
TYTGAT, G ;
VANDEVENTER, S .
LANCET, 1993, 342 (8864) :173-174
[9]  
Ellingsen EA, 2002, MED SCI MONITOR, V8, pBR149
[10]   EXPERIMENTAL-MODELS OF INFLAMMATORY BOWEL-DISEASE [J].
ELSON, CO ;
SARTOR, RB ;
TENNYSON, GS ;
RIDDELL, RH .
GASTROENTEROLOGY, 1995, 109 (04) :1344-1367