Lactobacillus salivariusalleviates inflammation via NF-κB signaling in ETEC K88-induced IPEC-J2 cells

被引:49
作者
Qiao, Jiayun [1 ]
Sun, Zeyang [1 ]
Liang, Dongmei [1 ]
Li, Haihua [2 ]
机构
[1] Tianjin Normal Univ, Coll Life Sci, Tianjin Key Lab Anim & Plant Resistance, Tianjin 300387, Peoples R China
[2] Tianjin Agr Univ, Coll Anim Sci & Vet Med, Tianjin Key Lab Agr Anim Breeding & Hlthy Husb, 22 Jinjing Rd, Tianjin 300384, Peoples R China
基金
中国国家自然科学基金;
关键词
ETEC K88; Inflammatory response; IPEC-J2; L; salivarius; INTESTINAL EPITHELIAL-CELLS; BARRIER FUNCTION; NEGATIVE REGULATORS; IMMUNE FUNCTION; IN-VITRO; PATHWAYS; PERFORMANCE; DYSFUNCTION; INHIBITION; EXPRESSION;
D O I
10.1186/s40104-020-00488-5
中图分类号
S8 [畜牧、 动物医学、狩猎、蚕、蜂];
学科分类号
0905 ;
摘要
Background EnterotoxigenicEscherichia coli(ETEC) K88 commonly colonize in the small intestine and keep releasing enterotoxins to impair the intestinal barrier function and trigger inflammatory reaction. AlthoughLactobacillus salivarius(L. salivarius) has been reported to enhance intestinal health, it remains to be seen whether there is a functional role ofL. salivariusin intestinal inflammatory response in intestinal porcine epithelial cell line (IPEC-J2) when stimulated with ETEC K88. In the present study, IPEC-J2 cells were first treated withL. salivariusfollowed by the stimulation of ETEC K88 for distinct time period. ETEC K88 adherent status, pattern recognition receptors (PRRs) mRNA, mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappa B) activation, the release of pro-inflammation cytokines and cell integrity were examined. Results Aside from an inhibited adhesion of ETEC K88 to IPEC-J2 cells,L. salivariuswas capable of remarkably attenuating the expression levels of interleukin (IL)-1 beta, tumor necrosis factor-alpha (TNF-alpha), IL-8, Toll-like receptor (TLR) 4, nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain-containing protein (NLRP) 3 and NLRP6. This alternation was accompanied by a significantly decreased phosphorylation of p38 MAPK and p65 NF-kappa B during ETEC K88 infection withL. salivariuspretreatment. Western blot analysis revealed thatL. salivariusincreased the expression levels of zona occludens 1 (ZO-1) and occludin (P< 0.05) in ETEC K88-infected IPEC-J2 cells. Compared with ETEC K88-infected groups, the addition ofL. salivariusas well as extra inhibitors for MAPKs and NF-kappa B to ETEC K88-infected IPEC-J2 cells had the capability to reduce pro-inflammatory cytokines. Conclusions Collectively, our results suggest thatL. salivariusmight reduce inflammation-related cytokines through attenuating phosphorylation of p38 MAPK and blocking the NF-kappa B signaling pathways. Besides,L. salivariusdisplayed a potency in the enhancement of IPEC-J2 cell integrity.
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页数:13
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