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Over-expression of IL-33 leads to spontaneous pulmonary inflammation in mIL-33 transgenic mice
Xiang, Zhiguang1; Chen, Wei1; Ravary, Steven1; Dong, Wei1; Zhang, Wei1; Mu, Rong2; Li, Zhanguo2; Zhang, Lianfeng1
关键词Il-33 Sst2 Transgenic Mice Cleavage Pulmonary Inflammation
刊名IMMUNOLOGY LETTERS
2010-07-08
DOI10.1016/j.imlet.2010.04.005
131期:2页:159-165
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Immunology
研究领域[WOS]Immunology
关键词[WOS]HUMAN MAST-CELLS ; AIRWAY INFLAMMATION ; CYTOKINE PRODUCTION ; HUMAN EOSINOPHILS ; ST2 RECEPTOR ; IN-VIVO ; INTERLEUKIN-33 ; PROTEIN ; MATURATION ; CASPASE-1
英文摘要

IL-33 plays an important role in inflammatory diseases including hypersensitive diseases like asthma, autoimmune diseases like rheumatoid arthritis, cardiovascular diseases like heart failure and neurodegenerative diseases like Alzheimer′s disease. Here we reported the generation of an IL-33 transgenic mouse, in which mouse IL-33 full-length cDNA was controlled under the CMV promoter. The transgenic IL-33 was released as a cleaved form with molecular weight of 18 kDa in pulmonary, nephritic, cardiac and pancreatic tissues in transgenic mice and the pI of 18 kDa peptide was about pH 3-5 on the 2D PAGE which was similar with the activated peptide of IL-33. Histological analysis showed massive airway inflammation with infiltration of eosinophils around bronchi and small blood vessels, hyperplasia of goblet cells and accumulation of mucus-like material in pulmonary tissue of transgenic mice. An increase of IL-5, IL-8, IL-13 and IgE was detected in bronchoalveolar lavage fluid (BALF) of transgenic mice, which are inflammatory factors. These findings suggest transgenic IL-33 could be cleaved and secreted in an activated form and play an important role in the pathogenesis of pulmonary inflammation. (C) 2010 Elsevier B.V. All rights reserved.

语种英语
WOS记录号WOS:000279703800008
项目编号200802036 ; 2009ZX09501-026 ; 2010CB529100
资助机构Ministry of Health, China ; National Science and Technology ; 973 projects
引用统计
被引频次:26[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/53683
专题北京大学第二临床医学院
北京大学第二临床医学院_风湿免疫科
作者单位1.Chinese Acad Med Sci, Peking Union Med Coll, Inst Lab Anim Sci, Key Lab Human Dis Comparat Med,Minist Hlth, Beijing 100021, Peoples R China
2.Peking Univ, Dept Rheumatol & Immunol, Peoples Hosp, Beijing 100044, Peoples R China
推荐引用方式
GB/T 7714
Xiang, Zhiguang,Chen, Wei,Ravary, Steven,et al. Over-expression of IL-33 leads to spontaneous pulmonary inflammation in mIL-33 transgenic mice[J]. IMMUNOLOGY LETTERS,2010,131(2):159-165.
APA Xiang, Zhiguang.,Chen, Wei.,Ravary, Steven.,Dong, Wei.,Zhang, Wei.,...&Zhang, Lianfeng.(2010).Over-expression of IL-33 leads to spontaneous pulmonary inflammation in mIL-33 transgenic mice.IMMUNOLOGY LETTERS,131(2),159-165.
MLA Xiang, Zhiguang,et al."Over-expression of IL-33 leads to spontaneous pulmonary inflammation in mIL-33 transgenic mice".IMMUNOLOGY LETTERS 131.2(2010):159-165.
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