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Immunobiotic Lactobacillus jensenii Elicits Anti-Inflammatory Activity in Porcine Intestinal Epithelial Cells by Modulating Negative Regulators of the Toll-Like Receptor Signaling Pathway

机译:免疫性詹森氏乳杆菌通过调节类似收费受体信号通路的负性调节剂,在猪肠道上皮细胞中激发抗炎活性。

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The effect of Lactobacillus jensenii TL2937 on the inflammatory immune response triggered by enterotoxigenic Escherichia coli (ETEC) and lipopolysaccharide (LPS) in a porcine intestinal epitheliocyte cell line (PIE cells) was evaluated. Challenges with ETEC or LPS elicited Toll-like receptor 4 (TLR4)-mediated inflammatory responses in cultured PIE cells, indicating that our cell line may be useful for studying inflammation in the guts of weaning piglets. In addition, we demonstrated that L. jensenii TL2937 attenuated the expression of proinflammatory cytokines and chemokines caused by ETEC or LPS challenge by downregulating TLR4-dependent nuclear factorκB (NF-κB) and mitogen-activated protein kinase (MAPK) activation. Furthermore, we demonstrated that L. jensenii TL2937 stimulation of PIE cells upregulated three negative regulators of TLRs: A20, Bcl-3, and MKP-1, deepening the understanding of an immunobiotic mechanism of action. L. jensenii TL2937-mediated induction of negative regulators of TLRs would have a substantial physiological impact on homeostasis in PIE cells, because excessive TLR inflammatory signaling would be downregulated. These results indicated that PIE cells can be used to study the mechanisms involved in the protective activity of immunobiotics against intestinal inflammatory damage and may provide useful information for the development of new immunologically functional feeds that help to prevent inflammatory intestinal disorders, including weaning-associated intestinal inflammation.
机译:评估了詹氏乳杆菌TL2937对猪肠上皮细胞系(PIE细胞)中由肠毒素性大肠杆菌(ETEC)和脂多糖(LPS)触发的炎症免疫反应的影响。 ETEC或LPS的挑战在培养的PIE细胞中引起了Toll样受体4(TLR4)介导的炎症反应,表明我们的细胞系可能对研究断奶仔猪的肠道炎症有用。此外,我们证明了詹氏乳杆菌TL2937通过下调TLR4依赖性核因子κB(NF-κB)和促分裂原激活的蛋白激酶(MAPK)激活来减弱由ETEC或LPS激发引起的促炎性细胞因子和趋化因子的表达。此外,我们证明了詹氏乳杆菌TL2937对PIE细胞的刺激上调了TLR的三个负调节剂:A20,Bcl-3和MKP-1,加深了对免疫生物作用机制的了解。 L. jensenii TL2937介导的TLRs负调节剂的诱导将对PIE细胞的体内稳态产生实质性的生理影响,因为过量的TLR炎性信号会被下调。这些结果表明,PIE细胞可用于研究免疫抗生素对肠道炎性损害的保护活性所涉及的机制,并可为开发有助于预防炎性肠道疾病(包括断奶相关肠道)的新型免疫功能饲料提供有用的信息。炎。

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