Bacterial interactions with cells of the intestinal mucosa: toll-like receptors and NOD2

被引:255
作者
Cario, E [1 ]
机构
[1] Univ Hosp Essen, Div Gastroenterol & Hepatol, Inst Grp 1, D-45147 Essen, Germany
关键词
D O I
10.1136/gut.2004.062794
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Toll-like receptors (TLR) and NOD2 are emerging as key mediators of innate host defence in the intestinal mucosa, crucially involved in maintaining mucosal as well as commensal homeostasis. Recent observations suggest new (patho-) physiological mechanisms of how functional versus dysfunctional TLRx/NOD2 pathways may oppose or favour inflammatory bowel disease (IBD). In health, TLRx signalling protects the intestinal epithelial barrier and confers commensal tolerance whereas NOD2 signalling exerts antimicrobial activity and prevents pathogenic invasion. In disease, aberrant TLRx and/or NOD2 signalling may stimulate diverse inflammatory responses leading to acute and chronic intestinal inflammation with many different clinical phenotypes.
引用
收藏
页码:1182 / 1193
页数:12
相关论文
共 158 条
[1]   The Crohn's disease protein, NOD2, requires RIP2 in order to induce ubiquitinylation of a novel site on NEMO [J].
Abbott, DW ;
Wilkins, A ;
Asara, JM ;
Cantley, LC .
CURRENT BIOLOGY, 2004, 14 (24) :2217-2227
[2]   TLR4 and MD-2 expression is regulated by immune-mediated signals in human intestinal epithelial cells [J].
Abreu, MT ;
Arnold, ET ;
Thomas, LS ;
Gonsky, R ;
Zhou, YH ;
Hu, B ;
Arditi, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (23) :20431-20437
[3]   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
[4]   Mutations in NOD2 are associated with fibrostenosing disease in patients with Crohn's disease [J].
Abreu, MT ;
Taylor, KD ;
Lin, YC ;
Hang, T ;
Gaiennie, J ;
Landers, CJ ;
Vasiliauskas, EA ;
Kam, LY ;
Rojany, M ;
Papadakis, KA ;
Rotter, JI ;
Targan, SR ;
Yang, HY .
GASTROENTEROLOGY, 2002, 123 (03) :679-688
[5]   Cutting edge: Different toll-like receptor agonists instruct dendritic cells to induce distinct th responses via differential modulation of extracellular signal-regulated kinase-mitogen-activated protein kinase and c-fos [J].
Agrawal, S ;
Agrawal, A ;
Doughty, B ;
Gerwitz, A ;
Blenis, J ;
Van Dyke, T ;
Pulendran, B .
JOURNAL OF IMMUNOLOGY, 2003, 171 (10) :4984-4989
[6]   Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3 [J].
Alexopoulou, L ;
Holt, AC ;
Medzhitov, R ;
Flavell, RA .
NATURE, 2001, 413 (6857) :732-738
[7]   MyD88-deficient mice develop severe intestinal inflammation in dextran sodium sulfate colitis [J].
Araki, A ;
Kanai, T ;
Ishikura, T ;
Makita, S ;
Uraushihara, K ;
Iiyama, R ;
Totsuka, T ;
Takeda, K ;
Akira, S ;
Watanabe, M .
JOURNAL OF GASTROENTEROLOGY, 2005, 40 (01) :16-23
[8]   TLR4 mutations are associated with endotoxin hyporesponsiveness in humans [J].
Arbour, NC ;
Lorenz, E ;
Schutte, BC ;
Zabner, J ;
Kline, JN ;
Jones, M ;
Frees, K ;
Watt, JL ;
Schwartz, DA .
NATURE GENETICS, 2000, 25 (02) :187-+
[9]  
Arnott IDR, 2005, GUT, V54, P308
[10]   NOD2/CARD15, TLR4 and CD14 mutations in Scottish and Irish Crohn's disease patients: evidence for genetic heterogeneity within Europe? [J].
Arnott, IDR ;
Nimmo, ER ;
Drummond, HE ;
Fennell, J ;
Smith, BRK ;
MacKinlay, E ;
Morecroft, J ;
Anderson, N ;
Kelleher, D ;
O'Sullivan, M ;
McManus, R ;
Satsangi, J .
GENES AND IMMUNITY, 2004, 5 (05) :417-425