Host lactosylceramide enhances Edwardsiella tarda infection,Cellular Microbiology

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Host lactosylceramide enhances Edwardsiella tarda infection
Cellular Microbiology ( IF 2.6 ) Pub Date : 2021-05-14 , DOI: 10.1111/cmi.13365
Kazuki Oishi ₁ , Moeri Morise ₂ , Linh Khanh Vo ₁ , Nhung Thi Tran ₂ , Daichi Sahashi ₂ , Rena Ueda-Wakamatsu ₂ , Wataru Nishimura ₂ , Masaharu Komatsu _{1,

2} , Kazuhiro Shiozaki _{1,

2}

Affiliation

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.

中文翻译：

宿主乳糖神经酰胺增强了爱德华氏菌感染

Edwardsiella tarda是一种革兰氏阴性细菌，对水产养殖造成经济损失。E. tarda与微域的相互作用是入侵的重要步骤，但微域中的靶分子仍未确定。在这里，我们发现腹膜内注射迟发性埃博拉改变了模型宿主青鳉 ( Oryzias latipes ) 中的脾鞘糖脂模式，并伴随着鞘糖脂代谢相关基因表达的改变，这表明鞘糖脂水平与迟发性埃博拉有关。感染。为了确定鞘糖脂在感染中的重要性，用甲基-β-环糊精处理鱼细胞系、具有大量乳糖神经酰胺 (LacCer) 和葡萄糖神经酰胺 (GlcCer) 的 DIT29 细胞以及具有少量这些脂质的 GAKS 细胞破坏微域。E. tarda感染在 DIT29 细胞中受到抑制，但在 GAKS 细胞中不受抑制，这表明微结构域 LacCer 和 GlcCer 参与了感染。DL-threo-1-phenyl-2-palmitoylamino-3-morpholino-1-propanol 是一种鞘糖脂合成抑制剂，可减轻 DIT29 细胞中的感染，而积累 LacCer 的过表达 Neu3 的 GAKS 细胞则增强了感染。迟发性大肠杆菌对 LacCer 具有结合能力，但对 GlcCer 不具有结合能力，并且 LacCer 预孵育降低了对鱼细胞的感染，可能是由于结合位点的掩蔽。目前的研究表明，LacCer 可能是E. tarda入侵的正调节剂。

更新日期：2021-05-14

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