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大肠杆菌菌株 Nissle 1917 的 K5 胶囊在刺激上皮细胞中 Toll 样受体 5、CD14、MyD88 和 TRIF 的表达以及通过丝裂原活化蛋白激酶途径诱导白细胞介素-8 表达方面非常重要。

The K5 capsule of Escherichia coli strain Nissle 1917 is important in stimulating expression of Toll-like receptor 5, CD14, MyD88, and TRIF together with the induction of interleukin-8 expression via the mitogen-activated protein kinase pathway in epithelial cells.

机构信息

Faculty of Life Sciences, University of Manchester, Michael Smith Building, Dover Street, Manchester M13 9PT, United Kingdom.

出版信息

Infect Immun. 2010 May;78(5):2153-62. doi: 10.1128/IAI.01406-09. Epub 2010 Feb 9.

Abstract

Escherichia coli strain Nissle 1917, which has been widely used as a probiotic for the treatment of inflammatory bowel disorders, expresses a K5 capsule, the expression of which is often associated with extraintestinal and urinary tract isolates of E. coli. Previously, it had been shown that the expression of a K5 capsule by Nissle 1917 was important in mediating interactions with epithelial cells and the extent of chemokine expression. In this paper, we show that infection with Nissle 1917 induces expression of Toll-like receptor 4 (TLR4) and TLR5 in Caco-2 cells and that maximal induction of TLR5 required the K5 capsule. In addition, purified K5 polysaccharide was capable of inducing expression of TLR5 and mCD14 and potentiated the activity of both TLR4 and TLR5 agonists to increase the proinflammatory response. Infection with Nissle 1917 also increased the expression of the adaptor molecules MyD88 and TRIF, which was K5 capsule dependent. By Western blot analysis, it was possible to show that induction of interleukin-8 by Nissle 1917 was predominantly through the mitogen-activated protein (MAP) kinase pathway and that expression of the K5 capsule was important for activation of the MAP kinase pathway. This paper provides new information on the function of the K5 capsule in mediating interactions between Nissle 1917 and epithelial cells and the mechanisms that underlie the probiotic properties of Nissle 1917.

摘要

大肠杆菌菌株 Nissle 1917 被广泛用作治疗炎症性肠病的益生菌,它表达 K5 荚膜,其表达通常与大肠杆菌的肠道外和尿路感染分离株有关。以前已经表明,Nissle 1917 表达 K5 荚膜对于介导与上皮细胞的相互作用和趋化因子表达的程度很重要。在本文中,我们表明 Nissle 1917 的感染诱导 Caco-2 细胞中 Toll 样受体 4 (TLR4) 和 TLR5 的表达,并且 TLR5 的最大诱导需要 K5 荚膜。此外,纯化的 K5 多糖能够诱导 TLR5 和 mCD14 的表达,并增强 TLR4 和 TLR5 激动剂的活性,以增加促炎反应。Nissle 1917 的感染还增加了衔接分子 MyD88 和 TRIF 的表达,这依赖于 K5 荚膜。通过 Western blot 分析,可以表明 Nissle 1917 诱导白细胞介素-8 的表达主要通过丝裂原激活蛋白 (MAP) 激酶途径,并且 K5 荚膜的表达对于 MAP 激酶途径的激活很重要。本文提供了有关 K5 荚膜在介导 Nissle 1917 与上皮细胞相互作用中的功能以及 Nissle 1917 益生菌特性的潜在机制的新信息。

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本文引用的文献

1
Regulation of colonic epithelial repair in mice by Toll-like receptors and hyaluronic acid.
Gastroenterology. 2009 Dec;137(6):2041-51. doi: 10.1053/j.gastro.2009.08.055. Epub 2009 Sep 2.
2
Up-regulation of the tight-junction protein ZO-1 by substance P and IGF-1 in A431 cells.
Cell Biochem Funct. 2009 Aug;27(6):388-94. doi: 10.1002/cbf.1587.
3
Immune responses of TLR5(+) lamina propria dendritic cells in enterobacterial infection.
J Gastroenterol. 2009;44(8):803-11. doi: 10.1007/s00535-009-0094-y. Epub 2009 Jun 24.
4
Lactobacilli stimulate the innate immune response and modulate the TLR expression of HT29 intestinal epithelial cells in vitro.
Int J Food Microbiol. 2009 Jul 31;133(1-2):86-93. doi: 10.1016/j.ijfoodmicro.2009.05.013. Epub 2009 May 15.
6
Pattern recognition receptors and control of adaptive immunity.
Immunol Rev. 2009 Jan;227(1):221-33. doi: 10.1111/j.1600-065X.2008.00731.x.
7
IKK/NF-kappaB signaling in intestinal epithelial cells controls immune homeostasis in the gut.
Mucosal Immunol. 2008 Nov;1 Suppl 1:S54-7. doi: 10.1038/mi.2008.53.
9
A microbial symbiosis factor prevents intestinal inflammatory disease.
Nature. 2008 May 29;453(7195):620-5. doi: 10.1038/nature07008.

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