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 × 108 CFU per well L. plantarum for 4 h, and then these cells were challenged with 0 or 1 × 108 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-1α (IL-1α), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumour necrosis factor-α (TNF-α) (P < 0·05) caused by ETEC K88. Additionally, L. plantarum inhibited the reduction in peroxisome proliferator-activated receptor-γ (PPAR-γ) expression caused by ETEC K88 (P < 0·05). 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-κB p65) (P < 0·05) 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-κB signalling pathways.
Conclusions: Lactobacillus plantarum inhibited the inflammatory response induced by ETEC K88 in IPEC-1 cells via modulating MAPK and NF-κB signalling.
Significance and impact of the study: This study elucidated the underlying mechanism in which probiotics protect against intestinal inflammation caused by ETEC K88.
Keywords: Lactobacillus plantarum; IPEC-1 cells; enterotoxigenic Escherichia coli K88; inflammatory response; mechanism.
© 2020 The Society for Applied Microbiology.