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鳗弧菌抗菌肽 1:一种可调节金黄色葡萄球菌脂磷壁酸诱导巨噬细胞炎症的橙色斑点石斑鱼抗菌肽。

Epinecidin-1: An orange-spotted grouper antimicrobial peptide that modulates Staphylococcus aureus lipoteichoic acid-induced inflammation in macrophage cells.

机构信息

Department of Anatomy and Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Marine Research Station, Institute of Cellular and Organismic Biology, Academia Sinica, Taiwan; The iEGG and Animal Biotechnology Center, National Chung Hsing University, Taichung, 402, Taiwan.

出版信息

Fish Shellfish Immunol. 2020 Apr;99:362-367. doi: 10.1016/j.fsi.2020.02.036. Epub 2020 Feb 19.

DOI:10.1016/j.fsi.2020.02.036
PMID:32084537
Abstract

Orange-spotted grouper (Epinephelus coioides) is among the most economically important of all fish species farmed in Asia. This species expresses an antimicrobial peptide called epinecidin-1 (EPI), which is considered to be a host defense factor due to its strong bacterial killing activity. Antimicrobial peptides usually possess both bacterial killing and immunomodulatory activity, however, the modulatory activity of EPI on Gram-positive bacterial lipoteichoic acids (LTA)-induced inflammation has not been previously reported. In this study, we found that EPI effectively suppressed LTA-induced production of proinflammatory factors in macrophages. Mechanistically, EPI attenuated LTA-induced inflammation by inhibiting Toll-like receptor (TLR) 2 internalization and subsequent downstream signaling (reactive oxygen species, Akt, p38 and Nuclear factor κB). However, protein abundance of TLR2 was not altered by EPI or LTA. Taken together, our findings reveal for the first time that EPI possesses inhibitory activity toward LTA-induced inflammation in macrophages.

摘要

橙点石斑鱼(Epinephelus coioides)是亚洲养殖的所有鱼类中最具经济价值的鱼类之一。该物种表达一种称为 Epinecidin-1(EPI)的抗菌肽,由于其强大的杀菌活性,被认为是一种宿主防御因子。抗菌肽通常具有杀菌和免疫调节活性,但 EPI 对革兰氏阳性菌脂磷壁酸(LTA)诱导的炎症的调节活性尚未见报道。在这项研究中,我们发现 EPI 可有效抑制巨噬细胞中 LTA 诱导的促炎因子的产生。在机制上,EPI 通过抑制 Toll 样受体(TLR)2 的内化及其后续的下游信号(活性氧、Akt、p38 和核因子κB)来减轻 LTA 诱导的炎症。然而,EPI 或 LTA 并未改变 TLR2 的蛋白丰度。总之,我们的研究结果首次揭示了 EPI 对巨噬细胞中 LTA 诱导的炎症具有抑制作用。

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