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脂肪酸结合蛋白通过中华绒螯蟹的Toll信号通路调节抗菌功能。

Fatty acid binding protein regulate antimicrobial function via Toll signaling in Chinese mitten crab.

作者信息

Wang Shichuang, Zhu Youting, Li Xuejie, Wang Qun, Li Jiayao, Li Weiwei

机构信息

Laboratory of Invertebrate Immunological Defense & Reproductive Biology, School of Life Science, East China Normal University, Shanghai, China.

College of Fisheries and Life Science, Shanghai Ocean University, Shanghai, China.

出版信息

Fish Shellfish Immunol. 2017 Apr;63:9-17. doi: 10.1016/j.fsi.2017.01.036. Epub 2017 Jan 25.

DOI:10.1016/j.fsi.2017.01.036
PMID:28131672
Abstract

Fatty acid binding proteins (FABPs) are members of the lipid binding protein superfamily and play crucial role in fatty acid transport and lipid metabolism. In macrophages, Adipocyte-type FABP is an important mediator of inflammation. However, the immune functions of FABPs in invertebrates are not well understood; here, we obtained the gene structure of Eriocheir sinensis FABP 3 and FABP 9 (EsFABP 3 and EsFABP 9), and compared with EsFABP 10. The mRNA expression profiles show that all three FABPs were significantly up-regulated in hemocytes after being challenged with bacteria. Of the three, EsFABP 3 was the most stable and also the most highly up-regulated. Further studies showed that knockdown of EsFABP 3 led to higher bacterial counts in the hemocyte culture medium and a significant decrease in the mRNA expression of some antimicrobial peptides following bacterial stimulation. Moreover, a subcellular study demonstrated that EsFABP 3 can affect nuclear translocation of the dorsal after Gram-positive bacterial stimulation in hemocytes. These findings support the notion that EsFABP 3 could inhibit bacterial proliferation by regulating antimicrobial peptides expression via the Toll signaling pathway.

摘要

脂肪酸结合蛋白(FABPs)是脂质结合蛋白超家族的成员,在脂肪酸转运和脂质代谢中起关键作用。在巨噬细胞中,脂肪细胞型FABP是炎症的重要介质。然而,FABPs在无脊椎动物中的免疫功能尚未得到充分了解;在此,我们获得了中华绒螯蟹FABP 3和FABP 9(EsFABP 3和EsFABP 9)的基因结构,并与EsFABP 10进行了比较。mRNA表达谱显示,在用细菌攻击后,所有三种FABPs在血细胞中均显著上调。在这三种蛋白中,EsFABP 3最稳定,上调幅度也最高。进一步研究表明,敲低EsFABP 3会导致血细胞培养基中细菌数量增加,并且在细菌刺激后一些抗菌肽的mRNA表达显著下降。此外,亚细胞研究表明,在革兰氏阳性细菌刺激血细胞后,EsFABP 3可以影响背侧蛋白的核转位。这些发现支持了EsFABP 3可以通过Toll信号通路调节抗菌肽表达来抑制细菌增殖的观点。

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