Parasitic Helminth Cystatin Inhibits DSS-Induced Intestinal Inflammation Via IL-10+F4/80+ Macrophage Recruitment.
10.3347/kjp.2011.49.3.245
- Author:
Sung Won JANG
1
;
Min Kyoung CHO
;
Mi Kyung PARK
;
Shin Ae KANG
;
Byoung Kuk NA
;
Soon Cheol AHN
;
Dong Hee KIM
;
Hak Sun YU
Author Information
1. Department of Parasitology, School of Medicine, Pusan National University, Yangsan 626-813, Korea. hsyu@pusan.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Clonorchis sinensis;
inflammatory bowel disease;
cystatin;
dextran sodium sulfate (DSS);
IL-10+F4/80+ macrophages
- MeSH:
Animals;
Antigens, Differentiation/analysis;
Clonorchis sinensis/*enzymology;
Colon/pathology;
Cystatins/*metabolism;
Cytokines/secretion;
Dextran Sulfate/toxicity;
Female;
Helminth Proteins/*metabolism;
Immunologic Factors/*metabolism;
Inflammation/chemically induced/*pathology;
Interleukin-10/analysis;
Intestines/*drug effects/pathology;
Lymph Nodes/immunology;
Macrophages/chemistry/*immunology;
Mice;
Mice, Inbred C57BL;
Severity of Illness Index;
Spleen/immunology
- From:The Korean Journal of Parasitology
2011;49(3):245-254
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.