Suppression of inflammatory cytokine secretion by granulocyte/monocyte adsorptive apheresis in active ulcerative colitis
Suppression of inflammatory cytokine secretion by granulocyte/monocyte adsorptive apheresis in active ulcerative colitis
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DOI：
10.1111/j.1774-9987.2005.00229.x
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发表时间：
2005-04-01
影响因子：
1.9
通讯作者：
Fujiyama, Y
中科院分区：
文献类型：
--
作者：
Andoh, A;Tsujikawa, T;Fujiyama, Y
为了阐明粒细胞/单核细胞吸附分离治疗溃疡性结肠炎（UC）患者的分子机制，研究了粒细胞/单核细胞吸附分离前后外周血单核细胞（PBMC）细胞因子反应的变化。纳入了4例活动性UC患者。所有患者均对粒细胞粒细胞吸附分离有反应。共分析了4例患者的20个疗程。在每次粒细胞/单核细胞吸附分离前后5min内从外周血静脉血中分离外周血单核细胞。用白细胞介素(IL)-1 β和肿瘤坏死因子(TNF)- α刺激细胞24 h，采用酶联免疫吸附试验（ELISA）检测细胞分泌的IL-8和IL-6水平。粒细胞/单核细胞吸附分离后，IL-1 β诱导的IL-8和IL-6分泌明显减少。分离后tnf - α诱导的IL-8分泌也显著减少，但tnf -a诱导的IL-6分泌无显著差异（P = 0.052）。综上所述，粒细胞/单核细胞吸附分离可下调PBMC中IL-1 β -和tnf α诱导的炎症反应。诱导对促炎细胞因子的低反应性可能是UC患者粒细胞/巨噬细胞吸附分离临床效果的重要因素。
To elucidate the molecular mechanisms involved in the therapeutic effects of granulocyte/monocyte adsorption apheresis, changes were investigated in the cytokine responses of peripheral blood mononuclear cells (PBMC) before and after granulocyte/monocyte adsorptive apheresis in ulcerative colitis (UC) patients. Four patients with active UC were enrolled. All patients responded to granulocytelmonocyte adsorptive apheresis. A total of 20 sessions of four patients were analyzed. Peripheral blood mononuclear cells were isolated from peripheral venous blood within 5 min before and after each session of granulocyte/monocyte adsorptive apheresis. The cells were stimulated with interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha for 24 h, and the secreted IL-8 and IL-6 levels were determined by enzyme-linked immunosorbent assay (ELISA). IL-1 beta-induced IL-8 and IL-6 secretion was significantly decreased after granulocyte/monocyte adsorptive apheresis. TNF-alpha-induced IL-8 secretion was also significantly decreased after apheresis, but there was no significant difference in TNF-a-induced IL-6 secretion (P = 0.052). In conclusion, granulocyte/monocyte adsorptive apheresis down-regulates the IL-1 beta- and TNF-alpha-induced inflammatory responses in PBMC. The induction of hyporesponsiveness to pro-inflammatory cytokines may be an important factor mediating the clinical effects of granulocyte/macrophage adsorptive apheresis in UC patients.