| Summary: | 碩士 === 國立成功大學 === 生物科技研究所 === 104 === That acute hepatopancreatic necrosis disease (AHPND) can cause up to 100% mortality in post-larvae shrimp makes it a costly problem for the shrimp industry. The etiology of AHPND is Vibrio parahaemolyticus (VP) which has a unique plasmid containing toxic genes, PirA and PirB. Our laboratory has already reported the basic pathogenesis of AHPND. However, the immune response of AHPND-infected shrimp remains unknown. In this study, we focus on two immune pathways, Toll and IMD, in shrimp during AHPND infection. In AHPND-infected shrimp, Toll- and IMD-regulated antimicrobial peptides (AMPs) were suppressed in the stomach (where VP colonized) and in hemocytes. However, in hepatopancreas (location with most profound lesion due to AHPND), these immune genes were significantly upregulated, especially IMD-regulated immune genes. To investigate the role of the IMD pathway in AHPND-infected shrimp, dsRNA was used to silence Relish, the key factor of the IMD pathway. Mortality was significantly higher in the Relish silencing group than the control group. We inferred that overexpression of the IMD pathway was caused by a host immune response against AHPND. This was apparently the first investigation of expression of immune genes in shrimp during AHPND infection. These results will provide the basis for future studies to elucidate interactions between the host immune network and AHPND.
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