Neutralization of complement component C5 ameliorates the development of dextran sulfate sodium (DSS)-colitis in mice.

Neutralization of complement component C5 ameliorates the development of dextran sulfate sodium (DSS)-colitis in mice.
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DOI:
10.3164/jcbn.12-63
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发表时间:
2013-01
影响因子:
2.4
通讯作者:
Andoh A
Andoh A
中科院分区:
医学4区
文献类型:
--
作者:
Aomatsu T;Imaeda H;Takahashi K;Fujimoto T;Kasumi E;Ban H;Bamba S;Yoden A;Tamai H;Fujiyama Y;Andoh A

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补体系统是先天免疫的有效效应子。为了阐明补体系统在炎症性肠病中的病理生理作用,我们评估了抗C5抗体对葡聚糖硫酸钠诱导的小鼠结肠炎发展的影响。在BALB/c小鼠中,每48 h腹腔内给予抗C5抗体(1 µg/只)诱导葡聚糖硫酸钠结肠炎。通过标准组织学程序评价组织样品。采用实时荧光定量PCR检测黏膜炎性细胞因子mRNA的表达。小鼠的体重减轻被抗C5抗体的施用完全阻断。抗C5抗体处理的小鼠的疾病活动指数显著低于葡聚糖硫酸钠处理的小鼠。结肠重量/长度比,组织学结肠炎评分和粘膜髓过氧化物酶活性显着低于抗C5抗体治疗的小鼠比葡聚糖硫酸钠小鼠。抗C5抗体给药显著降低了肿瘤坏死因子-α、白细胞介素-1 β和白细胞介素-6的粘膜mRNA表达。总之,补体系统在葡聚糖硫酸钠诱导的实验性结肠炎的发展中起作用。
The complement system is a potent effector of innate immunity. To elucidate the pathophysiological role of the complement system in inflammatory bowel disease, we evaluated the effects of anti-C5 antibodies on the development of dextran sulfate sodium-induced colitis in mice. Dextran sulfate sodium-colitis was induced in BALB/c mice with intraperitoneal administrations of anti-C5 antibodies (1 µg/body) every 48 h. Tissue samples were evaluated by standard histological procedures. The mucosal mRNA expression of the inflammatory cytokines was analyzed by real-time PCR. Body weight loss in the mice was completely blocked by the administration of anti-C5 antibody. The disease activity index was significantly lower in the anti-C5 antibody-treated mice than the dextran sulfate sodium mice. The colonic weight/length ratio, histological colitis score and mucosal myeloperoxidase activity were significantly lower in the anti-C5 antibody-treated mice than the dextran sodium sulfate mice. The administration of the anti-C5 antibody significantly reduced the mucosal expression of mRNAs for tumor necrosis factor-α, interleukin-1β and interleukin-6. In conclusion, the complement system plays a role in the development of dextran sodium sulfate-induced experimental colitis.
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