过敏性紫癜患儿单个核细胞凋亡与细胞因子、IGF-1的关系探讨
- 程涵蓉,文飞球,吴本清
作者信息
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Relationship between the apoptosis of mononuclear cell and the expression of cytokines and insulin-like growth factor-1 in patients with henoch-schonlein purpura
- CHENG Han-rong, WEN Fei-qiu, WU Ben-qing
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文章历史
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摘要
【目的】 探讨过敏性紫癜(henoch-schonlein purpura, HSP)患儿单个核细胞(mononuclear cell, MNCs)凋亡的变化,并检测周围血中细胞因子白细胞介素-8、白细胞介素-6、肿瘤坏死因子-α和胰岛素样生长因子Ⅰ的变化,探讨其对MNCs 凋亡的影响。 【方法】 采用流式细胞术检测36例HSP患儿和26名健康对照者MNCs 的凋亡情况,酶联免疫吸附试验(ELISA)检测细胞因子水平。 【结果】 HSP患儿MNCs 凋亡率明显高于健康对照组患儿,患儿周围血中所测因子水平均高于正常对照组。细胞因子、IGF-1升高的水平与MNCs的凋亡比例成正相关。 【结论】 HSP患儿MNCs 凋亡增加。存在免疫功能紊乱,炎性细胞因子、IGF-1产生过多可能是导致MNCs 凋亡增加的重要机制,通过适度调控细胞因子、IGF-1的分泌和MNCs 凋亡有可能会改善HSP预后。
Abstract
【Objective】 To observe the changes of mononuclear cell (MNCs) apoptosis and the level of inflammatory cytokines and IGF-1 in patients with henoch-schonlein purpura (HSP), and to study the relationship between them. 【Methods】 The apoptosis of MNCs in 36 patients with HSP and 22 healthy controls were determined with flow cytometry. The inflammatory cytokines and theIGF-1 were tested with ELISA method. 【Results】 The percentage of MNCs apoptosis in the patients with HSP was significantly higher than that of healthy controls. The levels of IL-8, TNF-α, IL-6, IGF-1 in patients with HSP were significantly higher than those of healthy controls, and the increased levels of inflammatory cytokines and IGF-1 in HSP patients were positively correlated to the percentage of MNCs apoptosis. 【Conclusions】 The data demonstrates that there is a promote apoptotic process of MNCs in active HSP. The high expression of inflammatory cytokines and IGF-1 may play an important role of promoting MNCs apoptosis which reduces the functional life span of MNCs. For this reason, modulating the expression of cytokines, IGF-1 and moderately controlling the apoptosis of MNCs may be a new therapeutic target for HSP treatment.
关键词
Key words
henoch-schonlein purpura / apoptosis / cytokines / mononuclear cell
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参考文献
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[2] Ozaltin F, Besbas N, Uckan D, et al. The role of apoptosis in childhood henoch-schonlein purpura[J]. Clinical rheumatology,2003,22(4/5):265-267.
[3] Carlo-del VG, Rosa P, Maria A, et al. Cytokine pattern and endothelium damage markers in Henoch-Schonlein purpura.[J]. Immunopharmacology and Immunotoxicology, 2008, 30(3):623-629.
[4] 胡亚美,江载芳.诸福棠实用儿科学(上册)[M].7版. 北京:人民卫生出版社,2005:688-690.
[5] Prais D, Amir J, Nussinovitch M. Recurrent henoch-schonlein purpura in children [J]. J Clin Rheumatol, 2007,13(10):25-28.
[6] Yang YH, Wang SJ, Chuang YH, et al. The level of IgA antibodies to human umbilical vein endothelial cells canbe enhancedby TNF-alpha treatment in children with Henoch-Schonlein purpura[J]. Clin Exp Immunol,2002,130:352-357.
[7] Yu YH, Pan KL, Li Q, et al. Roles of serum and urinary interleukins 13Ralpha2 and other cytokines in pediatricHenoch-Schonlein purpura[J]. Zhongguo Dang Dai Er Ke Za Zhi,2009,11(1):37-40.
[8] Duan B, Morel L. Role of B-1a cells in autoimmunity[J]. Autoimmun Rev,2006,5:403-408.
[9] Yang YH, Huang YH, Lin YL, et al. Circulating IgA from acute stage of childhood Henoch-Schonlein purpura can enhance endothelial interleukin (IL)-8 production through MEK/ERK signalling pathway[J]. Clin Exp Immunol,2006,144:247-253.
[10] Yildiz B, Kural N, Aydin BM, et al. Increased serum levels of insulin-like growth factor (IGF)-1 and IGF-binding protein-3 in Henoch-Schonlein purpura[J]. The Tohoku Journal of Experimental Medicine,2008,214(4):333-340.
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