A selected Lactobacillus rhamnosus strain promotes EGFR-independent Akt activation in an enterotoxigenic Escherichia coli K88-infected IPEC-J2 cell model
Enterotoxigenic Escherichia coli (ETEC) are important intestinal pathogens that cause diarrhea in humans and animals.Although probiotic bacteria may protect against ETEC-induced enteric infections, the underlying mechanisms are unknown.In this study, porcine intestinal epithelial J2 cells (IPEC-J2) were preincubated with and without Lactobacillus rhamnosus ATCC 7469 and then exposed to F4+ ETEC.Increases in TLR4 and NOD2 mRNA expression were observed at 3 h after F4+ ETEC challenge, but these increases were attenuated by L.rhamnosus treatment.Expression of TLR2 and NOD1 mRNA was upregulated in cells pre-treated with L.rhamnosus.Pre-treatment with L.rhamnosus counteracted F4+ ETEC-induced increases in TNF-α concentration.Increased PGE2.concentrations were observed in cells infected with F4+ ETEC and in cells treated with L.rhamnosus only.A decrease in phosphorylated epidermal growth factor receptor (EGFR) was observed at 3 h after F4+ ETEC challenge in cells treated with L.rhamnosus.Pre-treatment with L.rhamnosus enhanced Akt phosphorylation and increased ZO-1 and occludin protein expression.Our findings suggest that L.rhamnosus protects intestinal epithelial cells from F4+ ETEC-induced damage, partly through the anti-inflammatory response involving synergism between TLR2 and NOD1.In addition, L.rhamnosus promotes EGFR-independent Akt activation, which may activate intestinal epithelial cells in response to bacterial infection, in turn increasing tight junction integrity and thus enhancing the barrier function and restricting pathogen invasion.Pre-incubation with L.rhamnosus was superior to co-incubation in reducing the adhesion of F4+ ETEC to IPEC-J2 cells and subsequently attenuating F4+ ETEC-induced mucin layer destruction and suppressing apoptosis.Our data indicate that a selected L.rhamnosus strain interacts with porcine intestinal epithelial cells to maintain the epithelial barrier and promote intestinal epithelial cell activation in response to bacterial infection, thus protecting cells from the deleterious effects of F4+ ETEC.
ZHANG Wei ZHU Yaohong YANG Jincai YANG Guiyan ZHOU Dong WANG Jiufeng
Department of Veterinary Clinical Sciences, College of Veterinary Medicine, China Agricultural University,Beijing 100193 ,P.R.China
国内会议
中国畜牧兽医学会兽医内科与临床诊疗学分会第八届代表大会暨学术研讨会
大庆
英文
27-42
2015-07-22（万方平台首次上网日期，不代表论文的发表时间）