Neutralization of complement component C5 ameliorates the development of dextran sulfate sodium (DSS)-colitis in mice
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- Aomatsu Tomoki
- Department of Medicine, Shiga University of Medical Science Department of Pediatrics, Osaka Medical College
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- Imaeda Hirotsugu
- Department of Medicine, Shiga University of Medical Science
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- Takahashi Kenichiro
- Division of Mucosal Immunology, Graduate School, Shiga University of Medical Science
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- Fujimoto Takehide
- Division of Mucosal Immunology, Graduate School, Shiga University of Medical Science
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- Kasumi Eiji
- Department of Medicine, Shiga University of Medical Science
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- Ban Hiromitsu
- Department of Medicine, Shiga University of Medical Science
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- Bamba Shigeki
- Department of Medicine, Shiga University of Medical Science
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- Yoden Atsushi
- Department of Pediatrics, Osaka Medical College
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- Tamai Hiroshi
- Department of Pediatrics, Osaka Medical College
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- Fujiyama Yoshihide
- Department of Medicine, Shiga University of Medical Science
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- Andoh Akira
- Division of Mucosal Immunology, Graduate School, Shiga University of Medical Science
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抄録
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.
収録刊行物
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- Ｊｏｕｒｎａｌ ｏｆ Ｃｌｉｎｉｃａｌ Ｂｉｏｃｈｅｍｉｓｔｒｙ ａｎｄ Ｎｕｔｒｉｔｉｏｎ
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Ｊｏｕｒｎａｌ ｏｆ Ｃｌｉｎｉｃａｌ Ｂｉｏｃｈｅｍｉｓｔｒｙ ａｎｄ Ｎｕｔｒｉｔｉｏｎ 52 (1), 72-75, 2013
一般社団法人 日本酸化ストレス学会