Aquaculture Department, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang, China.
Aquaculture Department, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang, China.
Fish Shellfish Immunol. 2023 Feb;133:108557. doi: 10.1016/j.fsi.2023.108557. Epub 2023 Jan 18.
The emergence of the microsporidian, Enterocytospora artemiae, has caused serious economic losses to the aquaculture industry of Palaemonetes sinensis. The hepatopancreas is the main digestive and immune organ of P. sinensis, and the main site of E. artemiae infection. We used next-generation sequencing to determine the effects of E. artemiae parasitism on the hepatopancreas of P. sinensis at the transcriptome level. The hepatopancreas of P. sinensis was parasitized by E. artemiae, and 881 differentially expressed genes (DEGs) were obtained, of which 643 were upregulated and 238 were downregulated. These DEGs are mainly involved in DNA replication, transcription, translation, immunity, and metabolism. Among them, the cellular processes of DNA replication, transcription and translation are significantly strengthened, which may be related to the use of host ATP and nucleic acid by E. artemiae to achieve proliferation and damage to host cells to enhance DNA replication and repair. Moreover, to defend against E. artemiae, some immune genes related to antioxidation, such as glutathione metabolism, seleno compound metabolism, and cytochrome p450 2L1, were significantly upregulated, but simultaneously, tumor necrosis factor, NF-κB inhibitor α, and other immune-related genes were significantly down regulated, indicating that the parasitism of E. artemiae led to a significant decline in the immune defense ability of P. sinensis. From the perspective of metabolism, the metabolism-related DEGs of retinol, glycine, serine, and threonine metabolism, were significantly downregulated, resulting in insufficient nutrient absorption and decreased energy supply of the P. sinensis, which in turn affected their growth. The differential genes and pathways identified in this study can provide a reference basis to further elucidate the pathogenic mechanism of P. sinensis infected with E. artemiae and the prevention and control of microsporidia disease.
微孢子虫 Enterocytospora artemiae 的出现给中华绒螯蟹的水产养殖业造成了严重的经济损失。肝胰腺是中华绒螯蟹的主要消化和免疫器官,也是 E. artemiae 感染的主要部位。我们使用下一代测序技术在转录组水平上确定了 E. artemiae 寄生对中华绒螯蟹肝胰腺的影响。中华绒螯蟹的肝胰腺被 E. artemiae 寄生,获得了 881 个差异表达基因(DEGs),其中 643 个上调,238 个下调。这些 DEGs 主要参与 DNA 复制、转录、翻译、免疫和代谢。其中,DNA 复制、转录和翻译的细胞过程显著增强,这可能与 E. artemiae 利用宿主 ATP 和核酸来实现增殖以及破坏宿主细胞以增强 DNA 复制和修复有关。此外,为了抵御 E. artemiae,一些与抗氧化有关的免疫基因,如谷胱甘肽代谢、硒化合物代谢和细胞色素 p450 2L1,显著上调,但同时,肿瘤坏死因子、NF-κB 抑制剂 α 等免疫相关基因显著下调,表明 E. artemiae 的寄生导致中华绒螯蟹的免疫防御能力显著下降。从代谢的角度来看,视黄醇、甘氨酸、丝氨酸和苏氨酸代谢的代谢相关 DEGs 显著下调,导致中华绒螯蟹营养吸收不足,能量供应减少,从而影响其生长。本研究中鉴定的差异基因和途径可以为进一步阐明中华绒螯蟹感染 E. artemiae 的致病机制以及微孢子虫病的防治提供参考依据。