Department of Biotechnology and Bioindustry Sciences, National Cheng Kung University, Tainan, Taiwan.
Department of Biotechnology and Bioindustry Sciences, National Cheng Kung University, Tainan, Taiwan; International Center for Scientific Development of Shrimp Aquaculture, National Cheng Kung University, Tainan, Taiwan.
Fish Shellfish Immunol. 2022 Jul;126:271-282. doi: 10.1016/j.fsi.2022.05.035. Epub 2022 May 21.
Peritrophins are peritrophic membrane (PM) proteins that can interact with chitin fibers via chitin-binding domains. Peritrophins have essential roles in providing porosity and strength to the PM that lines the shrimp midgut. Acute hepatopancreatic necrosis disease (AHPND), caused by strains of V. parahaemolyticus, is known to initially colonize the shrimp stomach and simultaneously disrupt its structural barriers (e.g., cuticle or epithelial tissues) to reach the hepatopancreas. Although stomach and hepatopancreas were identified as target tissues involved in AHPND pathogenesis, our results indicated that peritrophin in peritrophic membrane has a crucial role in determining not only colonization of AHPND-causing bacteria but also their tissue distribution. As the interaction between LvPeritrophin (LvPT) and WSSV (white spot syndrome virus) is not well understood, we noted that LvPT expression was upregulated in shrimp stomach challenged with either WSSV or AHPND. In an in vitro pathogen binding assay, there was strong binding of recombinant LvPT WSSV and AHPND-causing V. parahaemolyticus, and various bacteria. Furthermore, dsRNA-mediated LvPT silencing inhibited WSSV gene expression and viral genome replication. However, downregulation of LvPT gene expression increased copies of AHPND-causing bacteria in shrimp digestive tract, and facilitated bacterial colonization in stomach. In conclusion, we speculated that LvPT might regulate bacterial colonization during AHPND, whereas in WSSV infection, LvPT silencing favored the host. Although recombinant LvPT had strong binding with WSSV, the precise role of LvPT in WSSV infection needs further investigation. These findings increased our understanding of host-pathogen interactions in AHPND and WSSV infection that can be applied in shrimp aquaculture for developing effective antibacterial and antiviral strategies.
围食膜蛋白是围食膜（PM）的蛋白质，可以通过几丁质结合域与几丁质纤维相互作用。围食膜蛋白在为虾中肠衬里的 PM 提供多孔性和强度方面起着重要作用。由副溶血弧菌引起的急性肝胰腺坏死病（AHPND）已知最初定植在虾胃中，并同时破坏其结构屏障（例如，外骨骼或上皮组织）以到达肝胰腺。尽管胃和肝胰腺被确定为参与 AHPND 发病机制的靶组织，但我们的结果表明，围食膜中的围食膜蛋白不仅在确定导致 AHPND 的细菌的定植方面起着关键作用，而且在其组织分布方面也起着关键作用。由于 LvPeritrophin（LvPT）与 WSSV（白斑综合征病毒）之间的相互作用尚不清楚，我们注意到在虾胃受到 WSSV 或 AHPND 攻击时，LvPT 表达上调。在体外病原体结合测定中，重组 LvPT WSSV 和引起 AHPND 的副溶血弧菌以及各种细菌的结合能力很强。此外，dsRNA 介导的 LvPT 沉默抑制了 WSSV 基因表达和病毒基因组复制。然而，LvPT 基因表达的下调增加了虾消化道中引起 AHPND 的细菌的拷贝数，并促进了细菌在胃中的定植。总之，我们推测 LvPT 可能在 AHPND 期间调节细菌定植，而在 WSSV 感染期间，LvPT 沉默有利于宿主。尽管重组 LvPT 与 WSSV 具有很强的结合能力，但 LvPT 在 WSSV 感染中的精确作用需要进一步研究。这些发现增加了我们对 AHPND 和 WSSV 感染中宿主-病原体相互作用的理解，可应用于虾养殖以开发有效的抗菌和抗病毒策略。
