嗜酸乳杆菌通过抑制仔猪中NF-κB和p38丝裂原活化蛋白激酶信号通路来减轻对产肠毒素大肠杆菌K88的炎症反应。
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.
作者信息
Li Haihua, Zhang Lei, Chen Longbin, Zhu Qi, Wang Wenjie, Qiao Jiayun
机构信息
Tianjin Institute of Animal Husbandry and Veterinary Medicine, Tianjin, China.
出版信息
BMC Microbiol. 2016 Nov 10;16(1):273. doi: 10.1186/s12866-016-0862-9.
BACKGROUND
A 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.
RESULTS
The 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.
CONCLUSIONS
Our findings suggested that L. acidophilus regulated inflammatory response to ETEC via impairing both NF-κB and MAPK signaling pathways in piglets.
背景
据报道，一种新分离的嗜酸乳杆菌菌株对仔猪脂多糖（LPS）刺激具有潜在的抗炎活性，而相关炎症反应的细节有限。在此，我们旨在分析嗜酸乳杆菌调节炎症反应的能力，并阐明其抗炎活性的相关机制。
结果
嗜酸乳杆菌明显抑制了产肠毒素大肠杆菌（ETEC）K88诱导的白细胞介素-1β（IL-1β）、白细胞介素-8（IL-8）和肿瘤坏死因子-α（TNF-α）的上调，同时白细胞介素-10（IL-10）显著增加。此外，嗜酸乳杆菌下调了ETEC攻击的仔猪脾脏和肠系膜淋巴结中模式识别受体Toll样受体（TLR）2和TLR4的表达，同时ETEC感染仔猪脾脏中核因子κB（NF-κB）p65和丝裂原活化蛋白激酶（MAPK）p38的磷酸化水平也降低。此外，嗜酸乳杆菌显著增加了ETEC攻击的仔猪脾脏中TLRs信号负调节因子的表达，包括Tollip、IRAK-M、A20和Bcl-3。
结论
我们的研究结果表明，嗜酸乳杆菌通过损害仔猪的NF-κB和MAPK信号通路来调节对ETEC的炎症反应。
Zotero 插件