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摘要来源：
j Anim Sci Biotechnol。 2020; 11：76。 EPUB 2020 8月3日。PMID： 32774852“> 32774852 Liang, Haihua Li
Article Affiliation:Jiayun Qiao
Abstract:BACKGROUND: Enterotoxigenic(ETEC) K88 commonly colonize in the small intestine and keep releasing enterotoxins to impair the intestinal barrier function and trigger inflammatory reaction.虽然（）据报道可以增强肠道健康，但在肠道猪上皮细胞系中是否存在功能性的作用尚待观察（IPEC-J2）用ETEC K88刺激时。在本研究中，首先通过刺激ETEC K88在不同的时间段内对IPEC-J2细胞进行处理。 ETEC K88粘附状态，模式识别受体（PRR）mRNA，有丝分裂原激活的蛋白激酶（MAPK）和核因子-κB（NF-κB）激活，促进细胞因子和细胞完整性的释放。 adhesion of ETEC K88 to IPEC-J2 cells,was capable of remarkably attenuating the expression levels of interleukin (IL)-1β, tumor necrosis factor-α(TNF-α), IL-8, Toll-like receptor (TLR) 4, nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain-containing protein (NLRP) 3 and NLRP6。这种交替伴随着ETEC K88感染期间P38 MAPK和p65 NF-κB的磷酸化显着降低。蛋白质印迹分析表明，表达水平已经ETEC K88感染的IPEC-J2细胞中的Zona Ouccludens 1（ZO-1）和occludin（<0.05）的s。 Compared with ETEC K88-infected groups, the addition ofas well as extra inhibitors for MAPKs and NF-κB to ETEC K88-infected IPEC-J2 cells had the capability to reduce pro-inflammatory cytokines.
CONCLUSIONS: Collectively, our results suggest thatmight reduce inflammation-related细胞因子通过减弱p38 MAPK的磷酸化并阻止NF-κB信号通路。此外，在增强IPEC-J2单元格完整性方面显示了效力。