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本文引用的文献

1
Evidence for Trypanosoma cruzi in adipose tissue in human chronic Chagas disease.在人类慢性恰加斯病的脂肪组织中发现克氏锥虫的证据。
Microbes Infect. 2011 Nov;13(12-13):1002-5. doi: 10.1016/j.micinf.2011.06.002. Epub 2011 Jun 21.
2
Adipokines in inflammation and metabolic disease.脂肪细胞因子与炎症和代谢性疾病。
Nat Rev Immunol. 2011 Feb;11(2):85-97. doi: 10.1038/nri2921. Epub 2011 Jan 21.
3
Weight loss and lipolysis promote a dynamic immune response in murine adipose tissue.体重减轻和脂肪分解促进了小鼠脂肪组织中的动态免疫反应。
J Clin Invest. 2010 Oct;120(10):3466-79. doi: 10.1172/JCI42845. Epub 2010 Sep 27.
4
Adipose tissue recruitment of leukocytes.脂肪组织招募白细胞。
Curr Opin Lipidol. 2010 Jun;21(3):172-7. doi: 10.1097/MOL.0b013e3283393867.
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Pattern recognition receptors and inflammation.模式识别受体与炎症。
Cell. 2010 Mar 19;140(6):805-20. doi: 10.1016/j.cell.2010.01.022.
6
Adiponectin deficiency exacerbates cardiac dysfunction following pressure overload through disruption of an AMPK-dependent angiogenic response.脂联素缺乏通过破坏 AMPK 依赖性血管生成反应加重压力超负荷后的心脏功能障碍。
J Mol Cell Cardiol. 2010 Aug;49(2):210-20. doi: 10.1016/j.yjmcc.2010.02.021. Epub 2010 Mar 4.
7
The road from discovery to clinic: adiponectin as a biomarker of metabolic status.从发现到临床之路:脂联素作为代谢状态的生物标志物
Clin Pharmacol Ther. 2009 Dec;86(6):592-5. doi: 10.1038/clpt.2009.155.
8
Chagas disease in Spain, the United States and other non-endemic countries.西班牙、美国和其他非流行国家的恰加斯病。
Acta Trop. 2010 Jul-Aug;115(1-2):22-7. doi: 10.1016/j.actatropica.2009.07.019. Epub 2009 Jul 29.
9
Perspectives on Trypanosoma cruzi-induced heart disease (Chagas disease).克氏锥虫所致心脏病(恰加斯病)的研究视角
Prog Cardiovasc Dis. 2009 May-Jun;51(6):524-39. doi: 10.1016/j.pcad.2009.02.001.
10
Transmission of Trypanosoma cruzi by heart transplantation.克氏锥虫通过心脏移植传播。
Clin Infect Dis. 2009 Jun 1;48(11):1534-40. doi: 10.1086/598931.

对感染克氏锥虫(巴西株)早期的脂肪组织反应。

Response of adipose tissue to early infection with Trypanosoma cruzi (Brazil strain).

机构信息

Department of Pathology, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY, USA.

出版信息

J Infect Dis. 2012 Mar 1;205(5):830-40. doi: 10.1093/infdis/jir840. Epub 2012 Jan 31.

DOI:10.1093/infdis/jir840
PMID:22293433
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3274374/
Abstract

Brown adipose tissue (BAT) and white adipose tissue (WAT) and adipocytes are targets of Trypanosoma cruzi infection. Adipose tissue obtained from CD-1 mice 15 days after infection, an early stage of infection revealed a high parasite load. There was a significant increase in macrophages in infected adipose tissue and a reduction in lipid accumulation, adipocyte size, and fat mass and increased expression of lipolytic enzymes. Infection increased levels of Toll-like receptor (TLR) 4 and TLR9 and in the expression of components of the mitogen-activated protein kinase pathway. Protein and messenger RNA (mRNA) levels of peroxisome proliferator-activated receptor γ were increased in WAT, whereas protein and mRNA levels of adiponectin were significantly reduced in BAT and WAT. The mRNA levels of cytokines, chemokines, and their receptors were increased. Nuclear Factor Kappa B levels were increased in BAT, whereas Iκκ-γ levels increased in WAT. Adipose tissue is an early target of T. cruzi infection.

摘要

棕色脂肪组织 (BAT) 和白色脂肪组织 (WAT) 以及脂肪细胞是克氏锥虫感染的靶标。在感染后 15 天的 CD-1 小鼠的脂肪组织中,即感染的早期阶段,发现寄生虫负荷很高。感染的脂肪组织中巨噬细胞显著增加,脂质积累减少,脂肪细胞大小、脂肪质量减少,脂肪分解酶表达增加。感染增加了 Toll 样受体 (TLR) 4 和 TLR9 的水平,以及丝裂原活化蛋白激酶途径的组成部分的表达。过氧化物酶体增殖物激活受体 γ 的蛋白和信使 RNA (mRNA) 水平在 WAT 中增加,而 BAT 和 WAT 中的脂联素的蛋白和 mRNA 水平显著降低。细胞因子、趋化因子及其受体的 mRNA 水平增加。核因子 Kappa B 水平在 BAT 中增加,而 Iκκ-γ 水平在 WAT 中增加。脂肪组织是克氏锥虫感染的早期靶标。