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一种由真菌多糖诱导的血管炎小鼠模型。

A murine model of vasculitis induced by fungal polysaccharide.

作者信息

Ohno Naohito

机构信息

Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.

出版信息

Cardiovasc Hematol Agents Med Chem. 2008 Jan;6(1):44-52. doi: 10.2174/187152508783329957.

DOI:10.2174/187152508783329957
PMID:18220720
Abstract

CAWS is a mannoprotein-beta-glucan complex obtained from the culture supernatant of the fungal pathogen Candida albicans. CAWS exhibits various biological activities, and induces prominent vasculitis of the aortic valve and the coronary arteries in mouse. A significant difference was noted in the susceptibility to and the degree of vasculitis induction among mouse lines. The difference in cytokine production among mouse lines may be strongly related to that difference, namely, IL-6, IFN-gamma and TNF-alpha presumably act as positive factors, and IL-10, as a negative regulator. On the other hand, as a structural component of the inducing substance, the presence or absence of beta-1,2-mannose residues was suggested to be closely related to the activity. An understanding of the molecular mechanisms underlying this model could lead to the conquest of many modern diseases. This model is also expected to be useful for the development of new therapeutic drugs for vasculitis and cardiovascular diseases.

摘要

CAWS是一种从真菌病原体白色念珠菌的培养上清液中获得的甘露糖蛋白 - β - 葡聚糖复合物。CAWS具有多种生物学活性,并可在小鼠体内诱导主动脉瓣和冠状动脉出现显著的血管炎。在不同品系小鼠对血管炎的易感性和诱导程度上观察到了显著差异。小鼠品系之间细胞因子产生的差异可能与该差异密切相关,即白细胞介素 - 6、干扰素 - γ和肿瘤坏死因子 - α可能作为正向因子起作用,而白细胞介素 - 10作为负调节因子。另一方面,作为诱导物质的结构成分,β - 1,2 - 甘露糖残基的存在与否被认为与活性密切相关。对该模型潜在分子机制的理解可能会攻克许多现代疾病。该模型也有望用于开发治疗血管炎和心血管疾病的新型治疗药物。

相似文献

1
A murine model of vasculitis induced by fungal polysaccharide.一种由真菌多糖诱导的血管炎小鼠模型。
Cardiovasc Hematol Agents Med Chem. 2008 Jan;6(1):44-52. doi: 10.2174/187152508783329957.
2
[Histopathological examination and analysis of mortality in DBA/2 mouse vasculitis induced with CAWS, a water-soluble extracellular polysaccharide fraction obtained from Candida albicans].[用从白色念珠菌中提取的水溶性细胞外多糖组分CAWS诱导DBA/2小鼠血管炎的组织病理学检查及死亡率分析]
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[Negative regulatory factor of CAWS (Candida albicans water-soluble fraction) -vasculitis in CBA/J mice as assessed by comparison with Bruton's tyrosine kinase-deficient CBA/N mice].[通过与布鲁顿酪氨酸激酶缺陷型CBA/N小鼠比较评估CAWS(白色念珠菌水溶性部分)-血管炎在CBA/J小鼠中的负调节因子]
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4
Recognition of alpha-mannan by dectin 2 is essential for onset of Kawasaki disease-like murine vasculitis induced by cell-wall polysaccharide.树突状细胞 2 识别α-甘露聚糖对于细胞壁多糖诱导的川崎病样小鼠血管炎的发生至关重要。
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Beta-mannosyl linkages negatively regulate anaphylaxis and vasculitis in mice, induced by CAWS, fungal PAMPS composed of mannoprotein-beta-glucan complex secreted by Candida albicans.β-甘露糖基连接可负向调节由CAWS诱导的小鼠过敏反应和血管炎,CAWS是由白色念珠菌分泌的甘露糖蛋白-β-葡聚糖复合物组成的真菌PAMPs。
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Murine model of Kawasaki disease induced by mannoprotein-beta-glucan complex, CAWS, obtained from Candida albicans.由从白色念珠菌获得的甘露糖蛋白 - β - 葡聚糖复合物CAWS诱导的川崎病小鼠模型。
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Characterization of a murine model with arteritis induced by Nod1 ligand, FK565: A comparative study with a CAWS-induced model.Nod1配体FK565诱导的小鼠动脉炎模型的特征:与CAWS诱导模型的比较研究
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Adeno-associated Virus Vector-mediated Interleukin-10 Induction Prevents Vascular Inflammation in a Murine Model of Kawasaki Disease.腺相关病毒载体介导的白细胞介素 10 诱导可预防川崎病小鼠模型中的血管炎症。
Sci Rep. 2018 May 15;8(1):7601. doi: 10.1038/s41598-018-25856-0.
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IL-10 is a negative regulatory factor of CAWS-vasculitis in CBA/J mice as assessed by comparison with Bruton's tyrosine kinase-deficient CBA/N mice.通过与布鲁顿酪氨酸激酶缺陷的CBA/N小鼠比较评估,白细胞介素-10是CBA/J小鼠中CAWS血管炎的负调节因子。
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Effects of Natural and Chemically Defined Nutrients on Candida albicans Water-soluble Fraction (CAWS) Vasculitis in Mice.天然及化学定义营养素对小鼠白色念珠菌水溶性成分(CAWS)血管炎的影响。
Med Mycol J. 2017;58(2):E47-E62. doi: 10.3314/mmj.16-00014.

引用本文的文献

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Kawasaki disease: pathophysiology and insights from mouse models.川崎病:病理生理学和来自小鼠模型的见解。
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2
A novel mouse model of coronary stenosis mimicking Kawasaki disease induced by Lactobacillus casei cell wall extract.一种模拟由干酪乳杆菌细胞壁提取物诱导的川崎病的冠状动脉狭窄的新型小鼠模型。
Exp Anim. 2020 Apr 24;69(2):233-241. doi: 10.1538/expanim.19-0124. Epub 2020 Jan 13.
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Role of Macrophage Migration Inhibitory Factor in Granulomatosis With Polyangiitis.
巨噬细胞移动抑制因子在肉芽肿性多血管炎中的作用。
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4
CAWS administration increases the expression of interferon γ and complement factors that lead to severe vasculitis in DBA/2 mice.CAWS 给药增加了干扰素 γ 和补体因子的表达,导致 DBA/2 小鼠发生严重的血管炎。
BMC Immunol. 2013 Sep 24;14:44. doi: 10.1186/1471-2172-14-44.
5
A Model of Left Ventricular Dysfunction Complicated by CAWS Arteritis in DBA/2 Mice.DBA/2小鼠左心室功能障碍合并CAWS动脉炎的模型
Int J Vasc Med. 2012;2012:570297. doi: 10.1155/2012/570297. Epub 2012 Jul 8.