肝肠孢子虫(EHP)是一种微孢子虫寄生虫,可感染凡纳滨对虾,引起严重的肝胰腺微孢子虫病(HPM),并造成重大的经济损失。本研究利用转录组学和代谢组学的联合分析来揭示EHP与其宿主之间的动态分子相互作用,太平洋白虾,在感染的早期和晚期。结果表明不同的免疫学,排毒,以及感染早期和晚期的抗氧化反应。在虾早期EHP感染期间,免疫激活与Ftz-F1和SEPs等基因的抑制相一致,可能有助于寄生虫逃避。相比之下,晚期感染显示出精细的免疫反应,吞噬作用增强Ftz-F1的下调和SEP表达的复苏.这个阶段的特点是上调的解毒和抗氧化反应,可能是对EHP累积效应的防御,促进稳定的宿主-病原体关系。在感染的后期,大多数免疫反应恢复到基线水平,而一些免疫基因仍然活跃。谷胱甘肽抗氧化系统在早期被抑制,但在后期被激活。这种现象可以促进EHP的早期入侵,同时帮助宿主减轻晚期感染引起的氧化损伤。值得注意的是,在多胺代谢中存在独特的事件。亚精胺合酶的持续上调和精胺水平的同时降低表明多胺在EHP发展中的潜在作用。在整个感染过程中,ATP合成酶和己糖激酶等基因的显着差异突出了对能量代谢途径的持续影响。此外,涉及色氨酸等氨基酸的生长相关途径,组氨酸,牛磺酸很早就被破坏了,可能有助于在感染的初始阶段观察到的生长抑制。总之,这些发现阐明了宿主之间的动态相互作用,凡纳滨对虾,和寄生虫,EHP,在感染期间。免疫反应的特异性相位差,能量代谢,和抗氧化过程强调了宿主和寄生虫之间的复杂关系。多胺代谢的破坏为理解EHP的增殖机制提供了新的视角。这些发现极大地促进了我们对EHP致病机制及其与宿主相互作用的理解。
Enterocytozoon hepatopenaei (EHP) is a microsporidian parasite that infects Litopenaeus vannamei, causing severe hepatopancreatic microsporidiosis (HPM) and resulting in significant economic losses. This study utilizes a combined analysis of transcriptomics and metabolomics to unveil the dynamic molecular interactions between EHP and its host, the Pacific white shrimp, during the early and late stages of infection. The results indicate distinct immunological, detoxification, and antioxidant responses in the early and late infection phases. During early EHP infection in shrimp, immune activation coincides with suppression of genes like Ftz-F1 and SEPs, potentially aiding parasitic evasion. In contrast, late infection shows a refined immune response with phagocytosis-enhancing down-regulation of Ftz-F1 and a resurgence in SEP expression. This phase is characterized by an up-regulated detoxification and antioxidant response, likely a defense against the accumulated effects of EHP, facilitating a stable host-pathogen relationship. In the later stages of infection, most immune responses return to baseline levels, while some immune genes remain active. The glutathione antioxidant system is suppressed early on but becomes activated in the later stages. This phenomenon could facilitate the early invasion of EHP while assisting the host in mitigating oxidative damage caused by late-stage infection. Notably, there are distinctive events in polyamine metabolism. Sustained up-regulation of spermidine synthase and concurrent reduction in spermine levels suggest a potential role of polyamines in EHP development. Throughout the infection process, significant differences in genes such as ATP synthase and hexokinase highlight the continuous influence on energy metabolism pathways. Additionally, growth-related pathways involving amino acids such as tryptophan, histidine, and taurine are disrupted early on, potentially contributing to the growth inhibition observed during the initial stages of infection. In summary, these findings elucidate the dynamic interplay between the host, Litopenaeus vannamei, and the parasite, EHP, during infection. Specific phase differences in immune responses, energy metabolism, and antioxidant processes underscore the intricate relationship between the host and the parasite. The disruption of polyamine metabolism offers a novel perspective in understanding the proliferation mechanisms of EHP. These discoveries significantly advance our comprehension of the pathogenic mechanisms of EHP and its interactions with the host.