Impact of Quorum Sensing Signal N-3-Oxododecanoyl Homoserine Lactone on Intestinal Porcine Enterocyte Cell

Impact of Quorum Sensing Signal N-3-Oxododecanoyl Homoserine Lactone on Intestinal Porcine Enterocyte Cell
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DOI:
10.1166/jbn.2023.3585
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发表时间:
2023-05
影响因子:
2.9
通讯作者:
Yang Yang-Yang;Congrong Wang;Yun Liu;Xinyan Ma;Pengpeng Xia;Mingxu Zhou;Qiangde Duan;G. Zhu
Yang Yang-Yang;Congrong Wang;Yun Liu;Xinyan Ma;Pengpeng Xia;Mingxu Zhou;Qiangde Duan;G. Zhu
中科院分区:
工程技术3区
文献类型:
--
作者:
Yang Yang-Yang;Congrong Wang;Yun Liu;Xinyan Ma;Pengpeng Xia;Mingxu Zhou;Qiangde Duan;G. Zhu

文献摘要

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群体感应(Quorum sensing,QS)是细菌中一种自诱导(autoinducer,AI)分子介导的信号传导系统。本研究探讨了一种群体感应信号分子N-3-氧代十二烷酰基高丝氨酸内酯(3 OC 12-HSL,同义词:OdDHL)对宿主细胞的直接影响,以进一步揭示QS系统在细菌与宿主细胞相互作用中的作用。以猪小肠上皮细胞(IPEC-J2)为模型细胞,用阿勒信号分子OdDHL刺激细胞,观察群体感应信号对宿主细胞的影响。结果表明,OdDHL对IPEC-J2细胞形态有明显影响,较低浓度和较短刺激时间可诱导细胞皱缩、变圆。MTT法显示OdDHL对IPEC-J2细胞活力无影响,提示细胞形态学改变并非信号分子毒性所致。用不同浓度和不同作用时间的OdDHL刺激IPEC-J2细胞,细胞形态学变化与阿勒浓度和作用时间呈正相关。细菌粘附实验表明,OdDHL能增强肠致病性大肠杆菌的粘附。coli对宿主细胞IPEC-J2的抗性,同时降低了其对宿主细胞的侵袭能力。荧光定量PCR和Western blot结果显示,紧密连接蛋白ZO-1的表达明显增加。与细胞骨架和细胞连接相关的多个基因的表达水平均受到OdDHL的调控。综上所述,OdDHL可直接影响IPEC-J2细胞的形态和紧密连接等生物学特性,降低宿主肠道防御能力,从而促进病原菌对仔猪肠道的粘附和损伤。本研究为进一步了解致病菌群调控的致病作用及其对疾病的预防提供了基础参考。
Quorum sensing (QS) is an autoinducer (AI) molecules mediated signaling system in bacteria. It is generally believed that bacteria can regulate their own characteristics or virulence through OS. This study investigated the direct effects of a quorum sensing signal molecule N-3-oxododecanoyl homoserine lactone (3OC12-HSL, synonyms: OdDHL) on host cells, to further reveal the function of QS system in the interaction between bacteria and host cells. Intestinal porcine enterocyte cell line (IPEC-J2) were used as model cells, and the AHL signal molecule OdDHL was used to stimulate the cells to observe the effect of quorum sensing signals on host cells. The results showed that OdDHL had an obvious effect on the morphology of IPEC-J2 cells, and a lower concentration and shorter time of stimulation could induce cell shrinkage and rounding. MTT assay revealed that OdDHL had no effect on IPEC-J2 cell viability, suggesting that the cell morphological changes were not from signaling molecule toxicity. Using different concentrations and different exposure times of OdDHL to stimulate IPEC-J2 cells, we demonstrated that changes in cell morphology were positively correlated with the concentration of AHL and exposure time. Bacterial adhesion assay showed that OdDHL could enhance the adhesion of enteropathogenic E. coli to host cell IPEC-J2, while reducing its invasion into host cell. Fluorescent quantitative PCR and Western blot revealed that the expression of tight junction protein ZO-1 was significantly increased. The expression levels of multiple genes that related to cytoskeletons and cell junction were all regulated by OdDHL. In conclusion, OdDHL could directly affect the biological characteristics of IPEC-J2 cells such as morphology and tight junction, reduce the intestinal defences of hosts, thereby promoting the adhesion and injury of pathogenic bacteria to the intestine of piglets. This study provides a basic reference for further understanding of the pathogenic role of regulating pathogenic bacterial populations and their prevention against diseases.