Abstract：
Enterocytozoon hepatopenaei (EHP) is the pathogen of hepatopancreatic microsporidiosis (HPM) in shrimp. The diseased shrimp Litopenaeus vannamei exhibits a slow growth syndrome, which causes severe economic losses. Herein, 4D label-free quantitative proteomics was employed to analyze the hepatopancreas of L. vannamei with a light (EHPptp2 < 103 copies/50 ng hpDNA, L group) and heavy (EHPptp2 > 104 copies/50 ng hpDNA, H group) load of EHP to better understand the pathogenesis of HPM. Exactly 786 (L group) and 1056 (H group) differentially expressed proteins (DEPs) versus the EHP-free (C group) control were mainly clustered to lipid metabolism, amino acid metabolism, and energy production processing. Compared with the L group, the H group exhibited down-regulation significantly in lipid metabolism, especially in the elongation and degradation of fatty acid, biosynthesis of unsaturated fatty acid, metabolism of α-linolenic acid, sphingolipid, and glycerolipid, as well as juvenile hormone (JH) degradation. Expression pattern analysis showed that the degree of infection was positively correlated with metabolic change. About 479 EHP proteins were detected in infected shrimps, including 95 predicted transporters. These findings suggest that EHP infection induced the consumption of storage lipids and the entire down-regulation of lipid metabolism and the coupling energy production, in addition to the hormone metabolism disorder. These were ultimately responsible for the stunted growth.
摘要：
肝肠孢子虫（EHP）是虾肝胰腺微孢子虫病（HPM）的病原体。患病的虾凡纳滨对虾表现出缓慢的生长综合征，造成严重的经济损失。在这里，4D无标记定量蛋白质组学用于分析南美白对虾乳杆菌的肝胰腺（EHPptp2＆lt;103拷贝/50nghpDNA，L组）和重（EHPptp2＆gt;104拷贝/50nghpDNA，H组)负荷EHP能更好地懂得HPM的病发机制。与无EHP（C组）对照相比，786（L组）和1056（H组）差异表达蛋白（DEPs）主要聚集到脂质代谢中，氨基酸代谢，和能源生产加工。与L组相比，H组脂质代谢显著下调，特别是脂肪酸的伸长和降解，不饱和脂肪酸的生物合成，α-亚麻酸的代谢，鞘脂，和甘油脂，以及幼体激素（JH）降解。表达模式分析显示感染程度与代谢变化呈正相关。在感染的虾中检测到约479个EHP蛋白，包括95个预测的运输者。这些发现表明，EHP感染诱导了储存脂质的消耗和脂质代谢的整体下调以及耦合能量的产生，除了激素代谢紊乱。这些最终导致了发育迟缓。
