Effects of intravenous immunoglobulin and aspirin treatment on the functions of circulating endothelial progenitor cells in children with Kawasaki disease
XU Ming-Guo, MEN Li-Na, ZU Ying, ZHAO Chun-Yu, MENG Xiang-Chun
Cardiovascular Center, Shenzhen Children′s Hospital, Shenzhen, Guangdong 518026, China. nihaomingguo@yahoo.com.cn
Abstract:OBJECTIVE: To study the effects of intravenous immunoglobulin (IVIG) and aspirin treatment on the functions of circulating endothelial progenitor cells (EPCs) in children with Kawasaki disease (KD) and possible mechanisms. METHODS: Blood samples were obtained in 10 children with KD before and 7 days after the treatment by IVIG and aspirin. MTT method, modified Boyden chamber method and cell culture plate adhesion method were used to assess the functions of EPCs, including proliferation, adhension and migration activities. The plasma levels of tumor necrosis factor-α (TNF-α) and high-sensitivity C reactive protein (hs-CRP) were also measured. RESULTS: The functions of circulating EPCs 7 days after IVIG and aspirin treatment were significantly improved. IVIG and aspirin treatment significantly reduced plasma TNF-α and hs-CRP concentrations. There was a significant linear regression relationship between the reduced plasma TNF-α and hs-CRP levels and the increased functions of circulating EPCs.ConclusionsIVIG and aspirin treatment can improve the functions of circulating EPCs, possibly through reducing plasma concentrations of TNF-α and hs-CRP.
XU Ming-Guo,MEN Li-Na,ZU Ying et al. Effects of intravenous immunoglobulin and aspirin treatment on the functions of circulating endothelial progenitor cells in children with Kawasaki disease[J]. CJCP, 2011, 13(12): 966-969.
[1]Brogan PA, Bose A, Burgner D, Shingadia D, Tulloh R, Michie C, et al. Kawasaki disease: an evidence based approach to diagnosis, treatment, and proposals for future research[J]. Arch Dis Child, 2002, 86(4): 286-290.
[2]Furukawa S, Matsubara T, Ichiyama T. Regulation of proinflammatory cytokine cascade in Kawasaki disease[J]. Nippon Rinsho, 2008, 66(2): 258-264.
[3]Lau AC, Duong TT, Ito S, Wilson GJ, Yeung RS. Inhibition of matrix metalloproteinase-9 activity improves coronary outcome in an animal model of Kawasaki disease[J]. Clin Exp Immunol, 2009,157(2): 300-309.
[4]Lau AC, Duong TT, Ito S, Yeung RS. Intravenous immunoglobulin and salicylate differentially modulate pathogenic processes leading to vascular damage in a model of Kawasaki disease[J]. Arthritis Rheum, 2009, 60(7): 2131-2141.
[6]Ahn SY, Jang GC, Shin JS, Shin KM, Kim DS. Tumor necrosis factor-alpha levels and promoter polymorphism in patients with Kawasaki disease in Korea[J].Yonsei Med J, 2003, 44(6): 1021-1026.
[7]Mitani Y, Sawada H, Hayakawa H, Aoki K, Ohashi H, Matsumura M, et al. Elevated levels of high-sensitivity C-reactive protein and serum amyloid-A late after Kawasaki disease: association between inflammation and late coronary sequelae in Kawasaki disease[J]. Circulation, 2005, 111(1): 38-43.
[8]Pinna GS, Kafetzis DA, Tselkas OI, Skevaki CL. Kawasaki disease: an overview[J].Curr Opin Infect Dis, 2008,21(3): 263-270.
[9]Chen J, Huang L, Song M, Yu S, Gao P, Jing J. C-reactive protein upregulates receptor for advanced glycation end products expression and alters antioxidant defenses in rat endothelial progenitor cells[J]. J Cardiovasc Pharmacol, 2009, 53(5): 359-367.
[10]Zhang Y, Herbert BS, Rajashekhar G, Ingram DA, Yoder MC, Clauss M, et al. Premature senescence of highly proliferative endothelial progenitor cells is induced by tumor necrosis factor-alpha via the p38 mitogen-activated protein kinase pathway[J]. Faseb J, 2009, 23(5):1358-1365.
[11]Asahara T, Murohara T, Sullivan A, Silver M, van der Zee R, Li T, et al. Isolation of putative progenitor endothelial cells for angiogenesis[J]. Science, 1997, 275(5302): 964-967.
[12]Hill JM, Zalos G, Halcox JP, Schenke WH, Waclawiw MA, Quyyumi AA, et al. Circulating endothelial progenitor cells, vascular function, and cardiovascular risk[J]. N Engl J Med, 2003, 348(7): 593-600.
[13]Werner N, Kosiol S, Schiegl T, Ahlers P, Walenta K, Link A, et al. Circulating endothelial progenitor cells and cardiovascular outcomes[J]. N Engl J Med, 2005, 353(10): 999-1007.
[16]Fukazawa R, Ogawa S. Long-term prognosis of patients with Kawasaki disease: at risk for future atherosclerosis?[J]. J Nippon Med Sch, 2009, 76(3): 124-133.
[18]He T, Smith LA, Harrington S, Nath KA, Caplice NM, Katusic ZS. Transplantation of circulating endothelial progenitor cells restores endothelial function of denuded rabbit carotid arteries[J]. Stroke, 2004, 35(10): 2378-2384.
[19]Werner N, Junk S, Laufs U, Link A, Walenta K, Bohm M, et al. Intravenous transfusion of endothelial progenitor cells reduces neointima formation after vascular injury[J]. Circ Res, 2003, 93(2): e17-e24.
[20]Hui-Yuen JS, Duong TT, Yeung RS. TNF-alpha is necessary for induction of coronary artery inflammation and aneurysm formation in an animal model of Kawasaki disease[J]. J Immunol, 2006, 176(10): 6294-6301.
[21]Musunuru K, Kral BG, Blumenthal RS, Fuster V, Campbell CY, Gluckman TJ, et al. The use of high-sensitivity assays for C-reactive protein in clinical practice[J]. Nat Clin Pract Cardiovasc Med, 2008, 5(10): 621-635.
[22]Nabata A, Kuroki M, Ueba H, Hashimoto S, Umemoto T, Wada H, et al. C-reactive protein induces endothelial cell apoptosis and matrix metalloproteinase-9 production in human mononuclear cells: Implications for the destabilization of atherosclerotic plaque[J]. Atherosclerosis, 2008, 196(1): 129-135.