Heparin stimulates biofilm formation ofEscherichia colistrain Nissle 1917

Heparin stimulates biofilm formation ofEscherichia colistrain Nissle 1917
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肝素刺激大肠杆菌 Nissle 生物膜形成 1917

DOI:
10.1007/s10529-020-03019-4
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发表时间:
2020
影响因子:
2.7
通讯作者:
Zhou Xianxuan
Zhou Xianxuan
中科院分区:
工程技术4区
文献类型:
--
作者:
Wu D;an;Li Xiaomei;Yu Yanying;Gong Bingxue;Zhou Xianxuan

文献摘要

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目的大肠杆菌Nissle 1917(ECN)是一种与病原菌竞争的肠道益生菌,已被用于缓解各种肠道功能障碍。肝素是一种富含在人和动物肠道粘膜中的硫酸化糖胺多糖,与细菌生物膜的形成密切相关。然而,肝素影响细菌生物膜形成的特性仍然不清楚。在本研究中,我们研究了肝素及其衍生物对ECN生物被膜形成的影响。加入天然肝素后,ECN生物被膜的形成是不加肝素时的6.9~10.8倍,分别是N-DS、2-O-DS、6-O-DS和N-/2-O-/6-O-DS的1.4、3.1、3.0和3.8倍。肝素解聚产生相对分子质量较小的链缩短的肝素片段。解聚的肝素不能促进ECN生物膜的形成。加入短链肝素片段的ECN生物膜的OD570值比天然肝素低8.7倍。此外,在添加肝素衍生物的情况下,对沙门氏菌的生物被膜形成进行了研究,结果与ECN生物被膜的形成情况一致。肝素的硫酸化和链长均有助于ECN生物膜的形成。这项研究增加了对肝素如何影响生物被膜形成的理解,表明肝素在促进益生菌在肠道定植中的潜在作用,这些益生菌可以拮抗病原体感染。
ObjectivesEscherichia colistrain Nissle 1917 (EcN), a gut probiotic competing with pathogenic bacteria, has been used to attenuate various intestinal dysfunctions. Heparin is a sulfated glycosaminoglycan enriched in the human and animal intestinal mucosa, which has a close connection with bacterial biofilm formation. However, the characteristics of heparin affecting bacterial biofilm formation remain obscure. In this study, we investigated the influence of heparin and its derivatives on EcN biofilm formation.ResultsHere, we found that heparin stimulated EcN biofilm formation in a dose-dependent manner. With the addition of native heparin, the EcN biofilm formation increased 6.9- to 10.8-fold than that without heparin, and was 1.4-, 3.1-, 3.0-, and 3.8-fold higher than that ofN-desulfated heparin (N-DS), 2-O-desulfated heparin (2-O-DS), 6-O-desulfated heparin (6-O-DS), andN-/2-O-/6-O-desulfated heparin (N-/2-O-/6-O-DS), respectively. Depolymerization of heparin produced chain-shortened heparin fragments with decreased molecular weight. The depolymerized heparins did not stimulate EcN biofilm formation. The OD570 value of EcN biofilm with the addition of chain-shortened heparin fragments was 8.7-fold lower than that of the native heparin. Furthermore, the biofilm formation ofSalmonella entericaserovar Typhimurium was also investigated with the addition of heparin derivatives, and the results were consistent with that of EcN biofilm formation.ConclusionsWe conclude that heparin stimulated EcN biofilm formation. Both the sulfation and chain-length of heparin contributed to the enhancement of EcN biofilm formation. This study increases the understanding of how heparin affects biofilm formation, indicating the potential role of heparin in promoting intestinal colonization of probiotics that antagonize pathogen infections.