Lactobacillus plantarum inhibited the inflammatory response induced by enterotoxigenic Escherichia coli K88 via modulating MAPK and NF-kappa B signalling in intestinal porcine epithelial cells
文献类型： 外文期刊
作者： Yang, J. 1 ; Qiu, Y. 1 ; Hu, S. 1 ; Zhu, C. 1 ; Wang, L. 1 ; Wen, X. 1 ; Yang, X. 1 ; Jiang, Z. 1 ;
作者机构： 1.Guangdong Acad Agr Sci, Key Lab Anim Nutr & Feed Sci South China, Guangdong Publ Lab Anim Breeding & Nutr, State Key Lab Livestock & Poultry,Minist Agr & Ru, Guangzhou, Peoples R China; Guangdong Acad Agr Sci, Inst Anim Sci, Guangdong Lab Lingnan Modern Agr, Guangzhou, Peoples R China
关键词： enterotoxigenic Escherichia coli K88; inflammatory response; IPEC‐ 1 cells; Lactobacillus plantarum; mechanism
期刊名称：JOURNAL OF APPLIED MICROBIOLOGY （ 影响因子：3.772； 五年影响因子：3.963 ）
ISSN： 1364-5072
年卷期：
页码：
收录情况： SCI
摘要： Aims To investigate the effects of Lactobacillus plantarum on inflammatory responses induced by ETEC K88 and explore the underlying molecular mechanisms. Methods and Results Intestinal porcine cells (IPEC-1) were incubated with 0 or 1 x 10(8) CFU per well L. plantarum for 4 h, and then these cells were challenged with 0 or 1 x 10(8) CFU per well ETEC K88 for 2 h. The results showed that pre-treatment of IPEC-1 cells with L. plantarum prevented the increases in the transcript abundance of interleukin-1 alpha (IL-1 alpha), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumour necrosis factor-alpha (TNF-alpha) (P < 0 center dot 05) caused by ETEC K88. Additionally, L. plantarum inhibited the reduction in peroxisome proliferator-activated receptor-gamma (PPAR-gamma) expression caused by ETEC K88 (P < 0 center dot 05). Moreover, L. plantarum pre-treatment downregulated the phosphorylation levels of c-Jun N-terminal kinase (JNK), extracellular regulated protein kinases 1 and 2 (ERK1/2) and p38 and the nuclear concentration of nuclear factor kappa B p65 (NF-kappa B p65) (P < 0 center dot 05) compared with ETEC K88 group. Silencing experiment further supported that the protective effect of L. plantarum P might mediated by suppression of ETEC-provoked activation of MAPK and NF-kappa B signalling pathways. Conclusions Lactobacillus plantarum inhibited the inflammatory response induced by ETEC K88 in IPEC-1 cells via modulating MAPK and NF-kappa B signalling. Significance and Impact of the Study This study elucidated the underlying mechanism in which probiotics protect against intestinal inflammation caused by ETEC K88.
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