Yuan Lanxin, Chu Bingxin, Chen Shiyan, Li Yanan, Liu Ning, Zhu Yaohong, Zhou Dong
College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
College of Veterinary Medicine, Northwest A&F University, Xianyang 712100, China.
Microorganisms. 2021 Nov 16;9(11):2363. doi: 10.3390/microorganisms9112363.
Enteropathogenic (EPEC) is a common zoonotic pathogen that causes acute infectious diarrhea. Probiotics like are known to help prevent pathogen infections. The protective effects of are closely associated with its secretory products exopolysaccharides (EPS). We explored the effects of the EPS from subsp. () on ameliorating the damage of an intestinal porcine epithelial cell line (IPEC-J2) during EPEC infection. Pretreatment with EPS alleviated EPEC-induced apoptosis through the restoration of cell morphology and the downregulation of protein expressions of cleaved-caspase 8, cleaved-caspase 3, and cleaved-PARP. EPS-mediated remission of apoptosis significantly improved cell viability during EPEC infection. EPEC infection also resulted in impaired autophagy, as demonstrated by decreased expressions of autophagy-related proteins Beclin 1, ATG5, and microtubule-binding protein light chain-3B (LC3B) and the increased expression of p62 through western blot analysis. However, EPS reversed these effects which indicated that EPS promoted autophagosome formation. Furthermore, EPS prevented the lysosome damage induced by EPEC as it enhanced lysosomal acidification and raised lysosome-associated protein levels, thus promoted autophagosome degradation. Our findings suggest that the amelioration of EPEC-induced cell damages by EPS is associated with the limitation of detrimental apoptosis and the promotion of autophagy flux.
肠致病性大肠杆菌（EPEC）是一种常见的人畜共患病原体，可引起急性感染性腹泻。已知像[具体益生菌名称未给出]这样的益生菌有助于预防病原体感染。[具体益生菌名称未给出]的保护作用与其分泌产物胞外多糖（EPS）密切相关。我们探讨了[具体益生菌名称未给出]亚种[具体亚种名称未给出]（[具体益生菌名称未给出]）的EPS对减轻EPEC感染期间猪肠上皮细胞系（IPEC-J2）损伤的影响。EPS预处理通过恢复细胞形态以及下调裂解的半胱天冬酶8、裂解的半胱天冬酶3和裂解的聚（ADP-核糖）聚合酶的蛋白表达来减轻EPEC诱导的细胞凋亡。EPS介导的细胞凋亡缓解在EPEC感染期间显著提高了细胞活力。通过蛋白质印迹分析表明，EPEC感染还导致自噬受损，表现为自噬相关蛋白Beclin 1、ATG5和微管结合蛋白轻链3B（LC3B）的表达降低以及p62的表达增加。然而，EPS逆转了这些作用，表明EPS促进了自噬体的形成。此外，EPS通过增强溶酶体酸化和提高溶酶体相关蛋白水平来防止EPEC诱导的溶酶体损伤，从而促进自噬体降解。我们的研究结果表明，EPS对EPEC诱导的细胞损伤的改善与有害细胞凋亡的限制和自噬通量的促进有关。
