Lactobacillus casei potentiates induction of oral tolerance in experimental arthritis

被引:74
|
作者
So, Jae-Seon [1 ]
Lee, Choong-Gu [1 ]
Kwon, Ho-Keun [1 ]
Yi, Hwa-Jung [1 ]
Chae, Chang-Suk [1 ]
Park, Jin-A [1 ]
Hwang, Ki-Chul [2 ]
Im, Sin-Hyeong [1 ,2 ]
机构
[1] Gwangju Inst Sci & Technol GIST, Dept Life Sci, Kwangju 500712, South Korea
[2] Yonsei Univ Coll Med, Div Cardiol, Cardiovasc Res Inst, Seoul 120752, South Korea
关键词
Rheumatoid arthritis; Collagen-induced arthritis; Lactobacillus casei; Probiotics; oral tolerance; Type; 11; collagen; Foxp3; Regulatory T cells;
D O I
10.1016/j.molimm.2008.07.038
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Probiotics have been shown to exert beneficial effects on modulation of diverse diseases. However, no information is available for the effect of probiotics in the induction of oral tolerance in autoimmune diseases. The main purpose of this study was to elucidate whether Lactobacillus casei (L. casei) affect the induction of oral tolerance in experimental rheumatoid arthritis (RA). Type 11 collagen (CII) alone or together with L. casei was orally administered into collagen-induced arthritis (CIA) rats, and its effects on the clinical and histopathological aspects of RA were investigated. Co-administration of L. casei with CII more effectively suppressed clinical symptoms, paw swelling, lymphocyte infiltration and destruction of cartilage tissues of experimental arthritis than the rats treated with CII alone. The enhanced therapeutic efficacy was associated with an increase in anti-inflammatory cytokines (IL-10 and TGF-beta) while decreasing pro-inflammatory cytokines (IL-1 beta, IL-2, IL-6, IL-12, IL-17, IFN-gamma and TNF-alpha). Co-administration of L. cosei with CII more effectively Suppressed CII-reactive T cell proliferation and the levels of Th1-type IgG isotypes (IgG2a and IgG2b), while up-regulating Foxp3 expression levels and the population of Foxp3(+) CD4(+) T cells. Our study provides evidence that L. casei could potentiate antigen-specific oral tolerance and suppress Th1-type immune responses of arthritic inflammation. (C) 2008 Elsevier Ltd. All rights reserved
引用
收藏
页码:172 / 180
页数:9
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