Jiangxi-OAI Joint Research Institute, Nanchang University, 235 Nanjing Donglu, Nanchang, Jiangxi, 330047, People's Republic of China.
Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi, 330004, People's Republic of China.
Appl Microbiol Biotechnol. 2021 May;105(10):4269-4284. doi: 10.1007/s00253-021-11240-y. Epub 2021 May 14.
Enterococcus faecium WEFA23 was previously found effectively against adherence and colonization of Listeria monocytogenes CMCC54007, which might be closely related to its surface layer protein (SLP). In this study, the protective of SLP of E. faecium WEFA23 against infection of L. monocytogenes CMCC54007 was systemically investigated. In vitro assay showed that SLP actively inhibited L. monocytogenes internalization into Caco-2 cell line, with decreasing mRNA level of pro-inflammation cytokines and virulence factors and restoring destroyed intestinal barrier. In vivo assay through excluding SLP of E. faecium WEFA23 by 5 M LiCl represented that SLP increased body weight, reduced mortality and cell counts of L. monocytogenes CMCC54007 in tissues of mice. Further researches showed that SLP protected against L. monocytogenes CMCC54007 infection by modulation of intestinal permeability and immunity, namely, it decreased fluorescein isothiocyanate (FITC)-Dextran in serum, ameliorated destroyed colon structure, and increased number of goblet cells and protein level of TJ protein (Claudin-1, Occludin, and ZO-1) in colon. For immunity, SLP decreased number of CD4 and CD8 T cells in liver, mRNA level, and content of pro-inflammatory factors IL-6, IL-1β, IFN-γ ,TNF-α, and NO, and restored the structure of liver and spleen. Key Points•SLP of E. faecium inhibited L. monocytogenes internalization and colonization•SLP of E. faecium ameliorated host intestinal barrier dysfunction•SLP of E. faecium decreased pro-inflammatory cytokines and cells.
屎肠球菌 WEFA23 先前被发现能有效抑制李斯特菌 CMCC54007 的黏附和定植,这可能与其表面层蛋白(SLP)密切相关。在本研究中,系统研究了屎肠球菌 WEFA23 的 SLP 对李斯特菌 CMCC54007 感染的保护作用。体外试验表明,SLP 能主动抑制李斯特菌内化进入 Caco-2 细胞系,降低促炎细胞因子和毒力因子的 mRNA 水平,并修复受损的肠道屏障。通过用 5 M LiCl 排除屎肠球菌 WEFA23 的 SLP 的体内试验表明,SLP 增加了体重,降低了李斯特菌 CMCC54007 在小鼠组织中的死亡率和细胞计数。进一步的研究表明,SLP 通过调节肠道通透性和免疫来保护免受李斯特菌 CMCC54007 的感染,即它降低了血清中的荧光素异硫氰酸酯(FITC)-葡聚糖,改善了受损的结肠结构,并增加了结肠中杯状细胞的数量和 TJ 蛋白(Claudin-1、Occludin 和 ZO-1)的蛋白水平。就免疫而言,SLP 减少了肝脏中 CD4 和 CD8 T 细胞的数量、mRNA 水平和促炎因子 IL-6、IL-1β、IFN-γ、TNF-α 和 NO 的含量,并恢复了肝脾结构。关键点:
SLP 抑制李斯特菌的内化和定植。
SLP 改善了宿主的肠道屏障功能障碍。
SLP 降低了促炎细胞因子和细胞。