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Parasitic Helminth Cystatin Inhibits DSS-Induced Intestinal Inflammation Via IL-$10^+F4/80^+$ Macrophage Recruitment
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  • Parasitic Helminth Cystatin Inhibits DSS-Induced Intestinal Inflammation Via IL-$10^+F4/80^+$ Macrophage Recruitment
  • Parasitic Helminth Cystatin Inhibits DSS-Induced Intestinal Inflammation Via IL-$10^+F4/80^+$ Macrophage Recruitment
저자명
Jang. Sung-Won,Cho. Min-Kyoung,Park. Mi-Kyung,Kang. Shin-Ae,Na. Byoung-Kuk,Ahn. Soon-Cheol,Kim. Dong-Hee,Yu. Hak-Sun
간행물명
The Korean journal of parasitology
권/호정보
2011년|49권 3호|pp.245-254 (10 pages)
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대한기생충학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Many immune down-regulatory molecules have been isolated from parasites, including cystatin (cystain protease inhibitor). In a previous study, we isolated and characterized Type I cystatin (CsStefin-1) of the liver fluke, Clonorchis sinensis. To investigate whether the CsStefin-1 might be a new host immune modulator, we induced intestinal inflammation in mice by dextran sodium sulfate (DSS) and treated them with recombinant CsStefin-1 (rCsStefin-1). The disease activity index (DAI) increased in DSS only-treated mice. In contrast, the DAI value was significantly reduced in rCsStefin-1-treated mice than DSS only-treated mice. In addition, the colon length of DSS only-treated mice was shorter than that of rCsStefin-1 treated mice. The secretion levels of IFN-${gamma}$ and TNF-${alpha}$ in the spleen and mesenteric lymph nodes (MLNs) were significantly increased by DSS treatment, but the level of TNF-${alpha}$ in MLNs was significantly decreased by rCsStefin-1 treatment. IL-10 production in both spleen and MLNs was significantly increased, and IL-$10^+F4/80^+$ macrophage cells were significantly increased in the spleen and MLNs of rCsStefin-1 treated mice after DSS treatment. In conclusion, rCsStefin-1 could reduce the intestinal inflammation occurring after DSS treatment, these effects might be related with recruitment of IL-10 secreting macrophages.