The Protective Effect of the Recombinant 53-kDa Protein of Trichinella spiralis on Experimental Colitis in Mice
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Linlin Du Hao Tang Zhongfu Ma Jia Xu Wenchao Gao Jiajia Chen Wenjia Gan Zhaoping Zhang Xinbing Yu Xingwang Zhou Xuchu Hu
- چاپ و سال / کشور: 2011
Description
Background Helminth infection has been proven to reduce the severity of experimental inflammatory bowel disease (IBD). The excretory-secretory proteins of helminths play an important role in the process of immunomodulation. Aims In the present study, we aimed to investigate the protective potential of recombinant Trichinella spiralis (TS) 53-kDa protein (rTsP53), a component of excretorysecretory proteins, on experimental colitis in mice. Methods BALB/c mice were treated subcutaneously with 50 lg rTsP53 three times at an interval of 5 days. Colitis was induced by intrarectal administration of 5 mg trinitrobenzene sulfonic acid (TNBS). Disease activities and macroscopic and microscopic scores were evaluated. To determine immune response provoked by rTsP53, we measured specific IgG1 and IgG2a values against rTsP53 in sera of mice. We also detected cytokine profiles as well as the markers of alternatively activated macrophages (M2) in mice. Results RTsP53 ameliorated significantly the disease activity index (DAI) as well as the macroscopic and microscopic scores. IgG1 but not IgG2a was the predominant specific antibody detected in the sera of immunized mice, indicating the potential of stimulating T-helper (Th) 2 bias response by rTsP3. Pre-treatment with rTsP53 decreased serum Th1 cytokines (TNF-a, IFN-c) and elevated serum levels of serum Th2 cytokines (IL-4, IL-13); it also decreased colonic Th1 cytokines (TNF-a, IL-6) and colonic regulatory cytokines (IL-10, TGF-b1). RTsP53 increased colonic M2 markers, arginase-1 (Arg-1), and found in inflammatory zone 1 (FIZZ1), compared to mice without rTsP53 pretreatment. Conclusions RTsP53 is a potential protective agent for IBD.
Dig Dis Sci DOI 10.1007/s10620-011-1689-8 Received: 29 November 2010 / Accepted: 21 March 2011
