Host lactosylceramide enhances <i>Edwardsiella tarda</i> infection
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- Kazuki Oishi
- The United Graduate School of Agricultural Sciences Kagoshima University Kagoshima Japan
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- Moeri Morise
- Faculty of Fisheries Kagoshima University Kagoshima Japan
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- Linh Khanh Vo
- The United Graduate School of Agricultural Sciences Kagoshima University Kagoshima Japan
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- Nhung Thi Tran
- Faculty of Fisheries Kagoshima University Kagoshima Japan
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- Daichi Sahashi
- Faculty of Fisheries Kagoshima University Kagoshima Japan
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- Rena Ueda‐Wakamatsu
- Faculty of Fisheries Kagoshima University Kagoshima Japan
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- Wataru Nishimura
- Faculty of Fisheries Kagoshima University Kagoshima Japan
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- Masaharu Komatsu
- The United Graduate School of Agricultural Sciences Kagoshima University Kagoshima Japan
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- Kazuhiro Shiozaki
- The United Graduate School of Agricultural Sciences Kagoshima University Kagoshima Japan
説明
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.
収録刊行物
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- Cellular Microbiology
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Cellular Microbiology 23 (9), 2021-05-30
Hindawi Limited
