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产生Hsp65通过IL-10和TLR2依赖性途径预防小鼠炎症性肠病。

Hsp65-Producing Prevents Inflammatory Intestinal Disease in Mice by IL-10- and TLR2-Dependent Pathways.

作者信息

Gomes-Santos Ana Cristina, de Oliveira Rafael Pires, Moreira Thaís Garcias, Castro-Junior Archimedes Barbosa, Horta Bernardo Coelho, Lemos Luísa, de Almeida Leonardo Augusto, Rezende Rafael Machado, Cara Denise Carmona, Oliveira Sérgio Costa, Azevedo Vasco Ariston Carvalho, Miyoshi Anderson, Faria Ana Maria Caetano

机构信息

Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil; Centro Universitário UNA, Belo Horizonte, Brazil.

Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil; Instituto Federal do Paraná, Palmas, Brazil.

出版信息

Front Immunol. 2017 Jan 30;8:30. doi: 10.3389/fimmu.2017.00030. eCollection 2017.

DOI:10.3389/fimmu.2017.00030
PMID:28194152
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5277002/
Abstract

Heat shock proteins (Hsps) are highly expressed at all sites of inflammation. As they are ubiquitous and immunodominant antigens, these molecules represent good candidates for the therapeutic use of oral tolerance in autoimmune and chronic inflammatory diseases. Evidences from human and animal studies indicate that inflammatory bowel disease (IBD) results from uncontrolled inflammatory responses to intestinal microbiota. Hsps are immunodominant proteins expressed by several immune cells and by commensal bacteria. Using an IBD mouse model, we showed that oral pretreatment with genetically modified that produces and releases Hsp65, completely prevented DSS-induced colitis in C57BL/6 mice. Protection was associated with reduced pro-inflammatory cytokines, such as IFN-γ, IL-6, and TNF-α; increased IL-10 production in colonic tissue; and expansion of CD4Foxp3 and CD4LAP regulatory T cells in spleen and mesenteric lymph nodes. This effect was dependent on IL-10 and toll-like receptor 2. Thus, this approach may open alternative options for long-term management of IBD.

摘要

热休克蛋白（Hsps）在所有炎症部位均高表达。由于它们是普遍存在且具有免疫显性的抗原，这些分子是自身免疫性疾病和慢性炎症性疾病中口服耐受治疗应用的良好候选者。来自人类和动物研究的证据表明，炎症性肠病（IBD）是由对肠道微生物群的失控炎症反应引起的。Hsps是由几种免疫细胞和共生细菌表达的免疫显性蛋白。使用IBD小鼠模型，我们表明用产生并释放Hsp65的基因修饰物进行口服预处理，可完全预防C57BL/6小鼠中DSS诱导的结肠炎。保护作用与促炎细胞因子如IFN-γ、IL-6和TNF-α的减少有关；结肠组织中IL-10产生增加；以及脾脏和肠系膜淋巴结中CD4Foxp3和CD4LAP调节性T细胞的扩增。这种效应依赖于IL-10和Toll样受体2。因此，这种方法可能为IBD的长期管理开辟替代选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b446/5277002/cbbf8f203f29/fimmu-08-00030-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b446/5277002/5acc1a79e5e5/fimmu-08-00030-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b446/5277002/81df7628862c/fimmu-08-00030-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b446/5277002/cbbf8f203f29/fimmu-08-00030-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b446/5277002/5acc1a79e5e5/fimmu-08-00030-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b446/5277002/81df7628862c/fimmu-08-00030-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b446/5277002/a4de0679b507/fimmu-08-00030-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b446/5277002/7c28c7663cf3/fimmu-08-00030-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b446/5277002/cbbf8f203f29/fimmu-08-00030-g005.jpg

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J Immunol Methods. 2015 Jun;421:36-43. doi: 10.1016/j.jim.2015.02.005. Epub 2015 Feb 20.
2
From field to fermentation: the origins of Lactococcus lactis and its domestication to the dairy environment.从田野到发酵罐：乳球菌属的起源及其对乳制品环境的驯化。
Food Microbiol. 2015 May;47:45-61. doi: 10.1016/j.fm.2014.11.001. Epub 2014 Nov 11.
3
Current overview of extrinsic and intrinsic factors in etiology and progression of inflammatory bowel diseases.
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4
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Neural Regen Res. 2024 Jul 1;19(7):1480-1488. doi: 10.4103/1673-5374.387974. Epub 2023 Nov 13.
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