Lactobacillus acidophilus alleviates the inflammatory response to enterotoxigenic Escherichia coli K88 via inhibition of the NF-κB and p38 mitogen-activated protein kinase signaling pathways in piglets

BMC Microbiology

Research Article

Lei Zhang¹  Qi Zhu¹  Longbin Chen¹  Wenjie Wang¹  Jiayun Qiao¹  Haihua Li¹ 

[1] Tianjin Institute of Animal Husbandry and Veterinary Medicine, Tianjin, China;

关键词: ETEC;    Inflammatory response;    Innate immunity;    L. acidophilus;    Mitogen-activated protein kinase;    Nuclear factor kappa B;    Toll-like receptor;   

DOI  :  10.1186/s12866-016-0862-9

 received in 2016-03-20, accepted in 2016-10-11,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundA newly isolated L. acidophilus strain has been reported to have potential anti-inflammatory activities against lipopolysaccharide (LPS) challenge in piglet, while the details of the related inflammatory responses are limited. Here we aimed to analysis the ability of L. acidophilus to regulate inflammatory responses and to elucidate the mechanisms involved in its anti-inflammatory activity.ResultsThe ETEC (enterotoxigenic Escherichia coli) K88-induced up-regulations of IL-1β, IL-8 and TNF-α were obviously inhibited by L. acidophilus while IL-10 was significantly increased. Moreover, L. acidophilus down-regulated pattern recognition receptors TLR (Toll-like receptor) 2 and TLR4 expression in both spleen and mesenteric lymph nodes of ETEC-challenged piglets, in accompanied with the reduced phosphorylation levels of nuclear factor kappa B (NF-κB) p65 and mitogen-activated protein kinase (MAPK) p38 as well in spleen of ETEC-infected piglets. Furthermore, L.acidophilus significantly increased the expression of the negative regulators of TLRs signaling, including Tollip, IRAK-M, A20 and Bcl-3 in spleen of ETEC-challenged piglets.ConclusionsOur findings suggested that L. acidophilus regulated inflammatory response to ETEC via impairing both NF-κB and MAPK signaling pathways in piglets.

【 授权许可】

CC BY   
© The Author(s). 2016