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Vet Immunol Immunopathol. 2016 Apr;172:55-63. doi: 10.1016/j.vetimm.2016.03.005. Epub 2016 Mar 5.

Protective effects of Lactobacillus plantarum on epithelial barrier disruption caused by enterotoxigenic Escherichia coli in intestinal porcine epithelial cells.

Author information

1
College of Animal Science, South China Agricultural University, Guangzhou 510642, China; Agro-biological Gene Research Center, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China.
2
Agro-biological Gene Research Center, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China.
3
Ministry of Agriculture Key Laboratory of Animal Nutrition and Feed Science (South China), Guangdong Public Laboratory of Animal Breeding and Nutrition, Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China.
4
Agro-biological Gene Research Center, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China; Ministry of Agriculture Key Laboratory of Animal Nutrition and Feed Science (South China), Guangdong Public Laboratory of Animal Breeding and Nutrition, Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China. Electronic address: jiangz28@qq.com.

Abstract

Tight junctions (TJs) play an important role in maintaining the mucosal barrier function and gastrointestinal health of animals. Lactobacillus plantarum (L. plantarum) was reported to protect the intestinal barrier function of early-weaned piglets against enterotoxigenic Escherichia coli (ETEC) K88 challenge; however, the underlying cellular mechanism of this protection was unclear. Here, an established intestinal porcine epithelia cell (IPEC-J2) model was used to investigate the protective effects and related mechanisms of L. plantarum on epithelial barrier damages induced by ETEC K88. Epithelial permeability, expression of inflammatory cytokines, and abundance of TJ proteins, were determined. Pre-treatment with L. plantarum for 6h prevented the reduction in transepithelial electrical resistance (TEER) (P<0.05), inhibited the increased transcript abundances of interleukin-8 (IL-8) and tumor necrosis factor (TNF-α) (P<0.05), decreased expression of claudin-1, occludin and zonula occludens (ZO-1) (P<0.05) and protein expression of occludin (P<0.05) of IPEC-J2 cells caused by ETEC K88. Moreover, the mRNA expression of negative regulators of toll-like receptors (TLRs) [single Ig Il-1-related receptor (SIGIRR), B-cell CLL/lymphoma 3 (Bcl3), and mitogen-activated protein kinase phosphatase-1 (MKP-1)] in IPEC-J2 cells pre-treated with L. plantarum were higher (P<0.05) compared with those in cells just exposed to K88. Furthermore, L. plantarum was shown to regulate proteins of nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. These results indicated that L. plantarum may improve epithelial barrier function by maintenance of TEER, inhibiting the reduction of TJ proteins, and reducing the expression of proinflammatory cytokines induced by ETEC K88, possibly through modulation of TLRs, NF-κB and MAPK pathways.

KEYWORDS:

Enterotoxigenic Escherichia coli K88; Epithelial barrier; IPEC-J2; Lactobacilli plantarum; Probiotic; Tight junction

PMID:
27032504
DOI:
10.1016/j.vetimm.2016.03.005
[Indexed for MEDLINE]

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