Receptor for advanced glycation end products (RAGE) regulates sepsis but not the adaptive immune response

Journal of Clinical Investigation

Volumn 113, Issue 11, 2004, Pages 1641-1650

  Liliensiek, Birgit ^a,b   Weigand, Markus A ^b   Bierhaus, Angelika ^b   Nicklas, Werner ^a   Kasper, Michael ^c   Hofer, Stefan ^b   Plachky, Jens ^b   Gröne, Herman Josef ^a   Kurschus, Florian C ^a   Schmidt, Ann Marie ^d   Yan, Shi Du ^d   Martin, Eike ^b   Schleicher, Erwin ^e   Stern, David M ^f   Hämmerling, Günter J ^a   Nawroth, Peter P ^b,e   Arnold, Bernd ^a  

^a GERMAN CANCER RESEARCH CENTER DKFZ   (Germany)

^b UNIVERSITY OF HEIDELBERG   (Germany)

^c DRESDEN UNIVERSITY OF TECHNOLOGY   (Germany)

^d Och Spine at New York Presbyterian Hospitals   (United States)

^e Department of Medicine IV ^*  (Germany)

^f MEDICAL COLLEGE OF GEORGIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADVANCED GLYCATION END PRODUCT; ADVANCED GLYCATION END PRODUCT RECEPTOR; ADVANCED GLYCOSYLATION END PRODUCT RECEPTOR; ADVANCED GLYCOSYLATION END-PRODUCT RECEPTOR; IMMUNOGLOBULIN RECEPTOR;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; HISTOPATHOLOGY; IMMUNOPATHOGENESIS; IMMUNOREACTIVITY; INFLAMMATION; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; SEPSIS; SEPTIC SHOCK; SIGNAL TRANSDUCTION; ANIMAL; CECUM; GENETICS; IMMUNE SYSTEM; IMMUNOLOGY; INJURY; METABOLISM; MOUSE MUTANT; PERITONITIS; TIME;

ANIMALS; CECUM; IMMUNE SYSTEM; MICE; MICE, KNOCKOUT; PERITONITIS; RECEPTORS, IMMUNOLOGIC; SEPSIS; SHOCK, SEPTIC; TIME FACTORS;

EID: 2942756123     PISSN: 00219738     EISSN: None     Source Type: Journal    
DOI: 10.1172/JCI200418704     Document Type: Article

References (62)

1. Zhang, G., and Ghosh, S. 2001. Toll-like receptor-mediated NF-ê activation: a phylogenetically conserved paradigm in innace immunity. J. Clin. Invest. 107:13-19.
2. Medzhitov, R., Preston Hurlburt, P., and Janeway, C.A.,Jr. 1997. A human homologue of the Drosophila toll protein signals activation of adaptive immunity. Nature. 388:394-397.
3. Modlin, R.L., Brightbill, H.D., and Godowski, P.J. 1999. The toll of innate immunity on microbial pathogens. N. Engl. J. Med. 340:1834-1835.
4. Ghosh, S., May, M.J., and Kopp, E.B. 1998. NF-κB and ReI proteins. Evolutionary conserved mediators of immune response. Annu. Rev. Immunol. 16:225-260.
5. Hoffmann, J.A., Kafatos, F.C., Janeway, C.A., and Ezekowitz, R.A. 1999. Phylogenetic perspectives in innate immunity. Science. 284:1313-1318.
6. Imler, J.L., and Hoffmann, J.A. 2000. Toll and Toll-like proteins: an ancient family of receptors signaling infection. Rev. Immunogenet. 2:294-304.
7. Kaiser, V., and Diamond, G. 2000. Expression of mammalian defensin genes. J. Leukoc. Biol. 68:779-784.
8. Kaisho, T., and Akira. S. 2001. Toll-like receptors and their signaling mechanism in innate immunity. Acta Odontol. Scand. 59:124-130.
9. Silverman, N., and Maniatis, T. 2001. NF-κB signaling pathways in mammalian and insect innate immunity. Genes Dev. 15:2321-2342.
10. Baeuerle, P.A. 1998. Proinfiammatory signaling: last pieces in the NF-κB puzzle? Curr. Biol 8:R19-R22.
11. Baeuerle, P.A., and Baltimore, D. 1996. NF-κB ten years after. Cell. 87:13-20.
12. Baeuerle, P.A., and Henkel, T. 1994. Function and activation of NF-κB in the immune system. Annu. Rev. Immun. 12:141-179.
13. Barnes, P.J., and Karin, M. 1997. Nuclear Factor-κB - A pivotai transcription factor in chronic inflammatory diseases. N. Engl. J. Med. 336:1066-1071.
14. Lawrence, T., Gilroy, D.W., Colville-Nash, P.R., and Willoughby, D.A. 2001. Possible new role for NF-κB in the resolution of inflammation. Nat. Med. 7:1291-1297.
15. Verma, I., Stevenson, J.K., Schwarz, E.M., van Antwerp, D., and Miyamoto, S. 1995. Rel/NF-κB/IκB family: intimate tales of association and dissociation. Genes Dev. 9:2723-2735.
16. Read, M.A., Whitley, M.Z., Williams, A.J., and Collins, T. 1994. NF-ΚB and IκBα: an inducible regulatory system in endothelial activation. J. Exp. Med. 179:503-512.
17. Beg, A.A., and Baldwin, A.S. 1993. The IKB proteins: multifunctional regulators of Rel/NF-κB transcriprion factors. Genes Dev. 7:2064-2070.
18. de-Martin, R., et al. 1993. Cytokine-inducible expression in endothelial cells of an Iκ Bα -like gene is regulated by NF-κ B. EMBO J. 12:2773-2779.
19. Schmidt, A.M., Yan, S.D., Van, S.F., and Stern, D.M. 2000. The biology of the receptor for advanced glycation end products and its ligands. Biochim. Biophys. Acta. 1498:99-111.
20. Schmidt, A.M., Yan, S.D., Van, S.F., and Stern, D.M. 2001. The multiligand receptor RAGE is a progression factor amplifying immune and inflammatory responses. J. Clin. Invest. 108:949-955.
21. Schmidt, A.M., et al. 1994. Cellular receptors for advanced glycation end products. Implications for induction of oxidant stress and cellular dysfunction in the pathogenesis of vascular lesions. Arterioscler. Thromb. 14:1521-1528.
22. Schmidt, A M., Yan, S.D., and Stern, D.M. 1995. The dark side of glucose. Nat. Med. 1:1002-1004.
23. Schmidt, A.M., and Stern, D.M. 2001. Receptor for AGE (RAGE) is a gene within the major histocompatibility class III region: implications for host response mechanisms in homeostasis and chronic disease. Front. Biosci. 6:D1151-D1160.
24. Sugaya, K., et al. 1994. Three genes in the human MHC class III region near the junction with the class H: gene for receptor of advanced glycosylation end products, PBX2 horneobox gene and a notch homolog, human counterpart of mouse mammary tumor gene int-3. Genomics. 23:408-419.
25. Bierhaus, A., et al. 2001. Diabetes-associated sustained activation of the transcription factor nuclear factor-κB. Diabetes. 50:2792-2808.
26. Hofmann, M.A., et al. 2002. RAGE and arthritis: the G82S polymorphism amplifies the inflammatory response. Genes Immun. 3:123-135.
27. Basta, G., et al. 2002. Advanced glycation end products activate endothelium through signal-transduction receptor RAGE: a mechanism for amplification of inflammatory responses. Circulation. 105:816-822.
28. Schmidt, A.M.. Hofmann, M., Taguchi, A., Van, S.D., and Stern, D.M. 2000. RAGE: a multiligand receptor contributing to the cellular response in diabetic vasculopathy and inflammation. Semin. Thromb. Hemost. 26:485-493.
29. Ritthaler, U., et al. 1995. Expression of receptors for advanced glycation end products in peripheral occlusive vascular disease. Am. J. Pathol. 146:688-694.
30. Abel, M., et al. 1995. Expression of receptors for advanced glycosylated end products in renal disease. Nepbrol. Dial. Transplant. 10:1662-1667.
31. Greten, J., et al. 1996. Expression of receptors for advanced glycation end products in uremia. Nephrol Dial Transplant. 11:786-790.
32. Tanji, N., et al. 2000. Expression of advanced glycation end products and their cellular receptor RAGE in diabetic nephropathy and nondiabetic renal disease. J. Am. Soc. Nephrol. 11:1656-1666.
33. Hofmann, M.A., et al. 2001. Hyperhomocysteinemia enhances vascular inflammation and accelerates atherosclerosis in a murine model. J. Clin. Invest. 107:675-683.
34. Schmidt, A.M., and Scern, D.M. 2000. Atherosclerosis and diabetes: the RAGE connection. Curr. Atheroscler. Rep. 2:430-436.
35. Park, L., et al. 1998. Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproducts. Nat. Med. 4:1025-1031.
36. Kisiinger, T., et al. 2000. Receptor for advanced glycation end products mediates inflammation and enhanced expression of tissue factor in vasculature of diabetic apolipoprotein E-null mice. Arterioscler. Thromb. Vasc. Biol. 21:905-910.
37. Hofmann, MA., et al. 1999. RAGE mediates a novel pro inflammatory axis: the cell surface receptor for SlOO/calgranulin polypeptides. Cell. 97:889-901.
38. Taguchi, A., et al. 2000. Blockade of RAGE-amphoterin signaling suppresses tumour growth and metastases. Nature. 405:354-360.
39. Hou, F.F., et al. 2002. Receptor for advanced glycation end products on human synovial fibroblasts: role in the pathogenesis of dialysis-related amyloidosis. J. Am. Soc. Nephrol. 13:1296-3106.
40. Lalla, E., Lamster, I.B., Stern, D.M., and Schmidt, A.M. 2001. Receptor for advanced glycation end products, inflammation, and accelerated periodontal disease in diabetes: mechanisms and insights into therapeutic modalities. Ann. Periodontol. 6:113-118.
41. Lue, L.F., et al. 2001. Involvement of microglial receptor for advanced glycation endproducts (RAGE) in Alzheimer's disease: identification of a cellular activation mechanism. Exp. Neurol. 171:29-45.
42. Goova, M.T., et al. 2001. Blockade of receptor for advanced glycation end-products restores effective wound healing in diabetic mice. Am. J. Pathol. 159:513-525.
43. Wautier, J.L., et al. 1996. Receptor-mediated endothelial cell dysfunction in diabetic vasculopathy. Soluble receptor for advanced glycation end products blocks hyperpermeability in diabetic rats. J. Clin. Invest. 97:238-243.
44. Anderson, K.V. 2000. Toll signaling pathways in the innate immune response. Curr. Opin. Immunol. 12:13-19.
45. Wang, H., et al. 1999. HMG-I as a late mediator of endotoxin lethality in mice. Science. 285:248-251.
46. Schlaeger, T.M., et. al. 1997. Uniform vascular-endothelial-cell-specific gene expression in both embryonic and adult transgenic mice. Proc. Natl. Acad. Sci. U. S. A. 94:3058-3063.
47. Kasper, M. 2003. Pulmonary pathology of knock-outs in mice lacking type I pneumocyte antigens. Ann. Anat. 185:144.
48. Van, S.S., et al. 2003. Suppression of experimental autoimmune encepbalomyelitis by selective blockade of encepha-litogenic T-cell infiltration of the central nervous system. Nat. Med. 9:287-293.
49. Bouchon, A., Facchetti, F., Weigand, M.A., and Colonna, M. 2001. TREM-I amplifies inflammation and is a crucial mediator of septic shock. Nature. 410:1103-1107.
50. Van, S.D., et al. 2000. Receptor-dependent cell stress and amyloid accumulation in systemic amyloidosis. Nat. Med. 6:643-651.
51. Gold, J.A., ec at 2003. CD40 contributes to lethality in acute sepsis: in vivo role for CD40 in innate immunity. Infect. Immun. 71:3521-3528.
52. Ulloa, L., et al. 2002. Ethyl pyruvate prevents lethality in mice with established letal sepsis and systemic inflammation. Proc. Natl. Acad. Sci. U. S. A. 99:12351-12356.
53. Chavakis, T., et al. 2003. The pattern recognition receptor (RAGE) is a counter receptor for leukocyte integrins: a novel pathway for inflammatory cell recruitment. J. Exp. Med. 198:1507-1515.
54. Newcomb, D., Bolgos, G., Green, L., and Remick, D. G. 1998. Antibiotic treatment influences outcome in murine sepsis: mediators of increased morbidity. Shock. 10:110-117
55. Constien, R., et al. 2001. Characterization of a novel EGFP reporter mouse to monitor ere recombination as demonstrated by a Tie2cre mouse line. Genesis. 30:36-44.
56. Schwenk, F., Baron, U. and Rajewsky, K. 1995. A cretransgenie mouse strain for the ubiquitous deletion of loxP-flanked gene segments including deletion in germ cells. Nucleic Acids Res. 23:5080-5081.
57. Sambrook, J., Fritsch, E.F., and Maniatis, T. 1989. Molecular cloning: a laboratory manual. 2nd edition. Cold Spring Harbor Laboratory Press. Plainview, New York, USA.
58. b mice: fine specificity and T cell receptor Vβ expression of encephalitogenic T cells. Eur. J. Immunol. 25:1951-1959.
59. Calandra, T., et al. 2000. Protection from septic shock by neutralization of macrophage migratory inhibitory factor. Nat. Med. 6:164-170.
60. Echtenacher, B, FaIk, W., Männel, D.N., and Krammer, P.H. 1990. Requirement of endogenous tumor necrosis factor/cachectin for recovery from experimental peritonitis. J. Immunol. 145:3762-3766.
61. Hofmann, M.A., et al. 1999. Peripheral blood mononuclear cells isolated from patients with diabetic nephropathy demonstrate increased activation of the oxidative-srress sensitive transcription factor NF-κB. Diabetologia. 42:222-232.
62. The R Development Core Team. 2003. The R reference manual: base package. Volumes 1 and 2. Network Theory Ltd. Bristol, United Kingdom.