Host lactosylceramide enhances Edwardsiella tarda infection

IF 2.6 2区 生物学 Q3 CELL BIOLOGY
Kazuki Oishi, Moeri Morise, Linh Khanh Vo, Nhung Thi Tran, Daichi Sahashi, Rena Ueda-Wakamatsu, Wataru Nishimura, Masaharu Komatsu, Kazuhiro Shiozaki
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引用次数: 4

Abstract

Edwardsiella tarda is a Gram-negative bacterium causing economic damage in aquaculture. The interaction of E. tarda with microdomains is an important step in the invasion, but the target molecules in microdomains remain undefined. Here, we found that intraperitoneal injection of E. tarda altered splenic glycosphingolipid patterns in the model host medaka (Oryzias latipes) accompanied by alteration of glycosphingolipid metabolism-related gene expressions, suggesting that glycosphingolipid levels are involved in E. tarda infection. To ascertain the significance of glycosphingolipids in the infection, fish cell lines, DIT29 cells with a high amount of lactosylceramide (LacCer) and glucosylceramide (GlcCer), and GAKS cells with a low amount of these lipids, were treated with methyl-β-cyclodextrin to disrupt the microdomain. E. tarda infection was suppressed in DIT29 cells, but not in GAKS cells, suggesting the involvement of microdomain LacCer and GlcCer in the infection. DL-threo-1-phenyl-2-palmitoylamino-3-morpholino-1-propanol, an inhibitor of glycosphingolipid-synthesis, attenuated the infection in DIT29 cells, while Neu3-overexpressing GAKS cells, which accumulated LacCer, enhanced the infection. E. tarda possessed binding ability towards LacCer, but not GlcCer, and LacCer preincubation declined the infection towards fish cells, possibly due to the masking of binding sites. The present study suggests that LacCer may be a positive regulator of E. tarda invasion.

Abstract Image

宿主乳糖神经酰胺增强迟发爱德华菌感染
迟发爱德华氏菌是一种革兰氏阴性菌,对水产养殖业造成经济损失。延迟芽孢杆菌与微结构域的相互作用是其入侵的重要步骤,但微结构域的靶分子尚未明确。本研究中,研究人员发现,在模型宿主米鳉鱼(Oryzias latipes)腹腔注射延迟棘球绦虫可改变其脾脏鞘糖脂模式,并伴有鞘糖脂代谢相关基因表达的改变,这表明鞘糖脂水平与延迟棘球绦虫感染有关。为了确定鞘糖脂在感染中的意义,我们用甲基β-环糊精破坏鱼细胞系、含有大量乳糖神经酰胺(LacCer)和葡萄糖神经酰胺(GlcCer)的DIT29细胞和含有少量这些脂质的GAKS细胞的微结构域。延迟性E.感染在DIT29细胞中受到抑制,而在GAKS细胞中没有,提示微结构域LacCer和glcer参与了感染。DL-threo-1-phenyl-2-palmitoylamino-3-morpholino-1-propanol是糖鞘脂合成抑制剂,对DIT29细胞的感染有减弱作用,而neu3过表达的GAKS细胞积累了LacCer,对感染有增强作用。迟缓E.对LacCer有结合能力,而对GlcCer没有,LacCer的预孵育抑制了对鱼细胞的感染,这可能是由于LacCer的结合位点被掩盖了。本研究提示LacCer可能是延迟芽孢杆菌入侵的积极调节因子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Cellular Microbiology
Cellular Microbiology 生物-微生物学
CiteScore
9.70
自引率
0.00%
发文量
26
审稿时长
3 months
期刊介绍: Cellular Microbiology aims to publish outstanding contributions to the understanding of interactions between microbes, prokaryotes and eukaryotes, and their host in the context of pathogenic or mutualistic relationships, including co-infections and microbiota. We welcome studies on single cells, animals and plants, and encourage the use of model hosts and organoid cultures. Submission on cell and molecular biological aspects of microbes, such as their intracellular organization or the establishment and maintenance of their architecture in relation to virulence and pathogenicity are also encouraged. Contributions must provide mechanistic insights supported by quantitative data obtained through imaging, cellular, biochemical, structural or genetic approaches.
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