Abstract OBJECTIVE: PPAR-γ is associated with the differentiation, apoptosis, proliferation and cytokine secretion of immunologic cells. This study investigated peripheral blood lymphoblastic PPAR-γ mRNA expression and its correlation with plasma IL-13 contents in children with acute idiopathic thrombocytopenic purpura (ITP). METHODS: Fifty-three children with acute ITP who were in line with the standard test between September 2007 and July 2008 were enrolled. Fifty healthy children during the same period were used as the control group. PPAR-γ mRNA expression in peripheral blood lymphocytes were detected by RT-PCR. Plasma IL-13 contents were detected using ELISA. RESULTS: PPAR-γ mRNA expression in peripheral blood lymphocytes from acute ITP children were significantly higher than that in the control group (0.78 ± 0.03 vs 0.52 ± 0.05; P<0.05). Plasma IL-13 contents in children with acute ITP were also significantly higher than those in the control group (160.21 ± 34.26 pg / mL vs 121.42 ± 12.69 pg / mL; P<0.05). There was a positive correlation between plasma IL-13 level and lymphoblastic PPAR-γmRNA expression in children with ITP (r=0.89, P<0.05). CONCLUSIONS: PPAR-γ mRNA expression in peripheral blood lymphocytes increased and were positively correlated with plasma IL-13 contents in children with acute ITP, suggesting that PPAR-γ and IL-13 might participate in the pathogenesis of acute ITP.［Chin J Contemp Pediatr, 2009, 11 (5):367-370］
JIN Cheng-Qiang,LIU Fang,XIAO Hong et al. Correlation of lymphoblastic PPAR-γ mRNA expression with plasma IL-13 contents in children with acute idiopathic thrombocytopenic purpura[J]. 中国当代儿科杂志, 2009, 11(05): 367-370.
JIN Cheng-Qiang,LIU Fang,XIAO Hong et al. Correlation of lymphoblastic PPAR-γ mRNA expression with plasma IL-13 contents in children with acute idiopathic thrombocytopenic purpura[J]. CJCP, 2009, 11(05): 367-370.
［1］Medeiros D, Buchanan GR. Current controversies in the management of idiopathic thrombocytopenic purpura during childhood［J］. Pediatr Clin North Am, 1996, 43(3):757-772.
［3］Cines DB, McMillan R. Management of adult idiopathic thrombocytopenic purpura［J］. Annu Rev Med, 2005, 56:425-442.
［4］McMilan R. Classical management of refractory adult immune (idiopathic) thrombocytopenic purpura［J］. Blood Rev, 2002, 16(1): 51-55.
［5］Zhang X, Rodriguez-Galan MC, Subleski JJ. Peroxisome proliferator-activated receptor-gamma and its ligands attenuate biologic functions of human natural killer cells［J］. Blood, 2004, (10):3276-84.
［6］Kanoh M, Uetani T, Sakan H. A two-step model of T cell subset commitment: antigen-independent commitment of T cells before encountering nominal antigen during pathogenic infections［J］. Int Immunol, 2002, 14(6):567-575.
［7］Iruretagoyena MI, Sepúlveda SE, Lezana JP, Hermoso M, Bronfman M, Gutierrez MA, et al. Inhibition of nuclear factor-B enhances the capacity of immature dendritic cells to induce antigen-specific tolerance in experimental autoimmune encephalomyelitis［J］. JPET, 2006, 318(1):59-67.
［8］Inoue K, Takanoa H, Yanagisawaa R.ffects of 15-deoxy-delta(12,14)-prostaglandin J2 on nuclear localization of GATA-3 in the murine lung in the presence of lipopolysaccharide［J］. Arzneimittelforschung, 2005, 55(3):167-171.
［9］Kosuge H, Haraguchi G, Koga N. Pioglitazone prevents acute and chronic cardiac allograft rejection［J］. Circulation, 2006, 113(22):2613-2622.
［10］Coste A, Lagane C, Filipe C, Authier H, Galès A, Bernad J, et al. IL-13 attenuates gastrointestinal candidiasis in normal and immunodeficient RAG-2-/-mice via peroxisome proliferator-activated receptor-r activation［J］. J Immunol, 2008, 180(7):4939-4947.
［11］Steffel J, Lüscher TF, Tanner FC. Tissue factor in cardiovascular diseases molecular mechanisms and clinical implications［J］. Circulation, 2006, 113(5):722-731.
［12］Waldo SW, Li Y, Buono C, Zhao B, Billings EM, Chang J, et al. Heterogeneity of human macrophages in culture and in atherosclerotic plaques［J］. Am J Pathd, 2008, 172(4):1112-1116.
［13］Marion-Letellier R, Butler M, Déchelotte P, Playford RJ, Ghosh S. Comparison of cytokine modulation by natural peroxisome proliferatoractivated receptor γ ligands with synthetic ligands in intestinal-like Caco-2 cells and human dendritic cells-potential for dietary modulation of peroxisome proliferator-activated receptor γ in intestinal inflammation［J］. Am J Clin Nutr, 2008, 87(4):939-948.
