In crustacean, hemocytes are known as crucial components of crustaceans’ innate immunity against pathogens. Drastic hemocytes reduction during infectious disease is apparently related to disease severity and calls for a health status evaluation and aquaculture management. The molecular pathogenesis of hemocytes loss during bacterial infection was elucidated with VP_AHPND challenged in M. rosenbergii. We report herein a correlation between hemocyte loss and the pathogenicity and aggressive immune response in hematopoietic tissues of moribund M. rosenbergii. In this study, adult freshwater prawn was administered an LC₅₀ dose of VP_AHPND; bacterial clearance ensued, and success was reached within 24 h. Hemocytes increased in survival, yet drastically decreased in moribund prawn. Pathological analysis of hematopoietic tissue of moribund prawn showed apparent abnormal signs, including the presence of bacteria, a small number of mitotic cells, cellular swelling, loosening of connective tissue, and karyorrhectic nuclei cells. A significant upregulation of a core apoptotic machinery gene, caspase-3, was detected in hematopoietic tissue of moribund shrimp, but not in those of Escherichia coli DH5α (non-pathogenic bacteria) and VP_AHPND survival prawn. The highest level was found in the moribund group, which confirms the occurrence of apoptosis in this hematopoietic tissue. Further, our results suggest that hematopoietic tissue damage may arise from inflammation triggered by an aggressive immune response. Immune activation was indicated by the comparison of immune-related gene expression between controls, E. coli (DH5α)-infected (non-pathogenic), and VP_AHPND-infected survival groups with moribund prawn. RT-PCR revealed a significant upregulation of all genes in hematopoietic tissues and hemocytes within 6–12 h and declined by 24 h. This evident related to the almost VP_AHPND are clearance in survival and E. coli (DH5α) challenged group in contrast with drastic high expression was determined in moribund group. We conclude that a reduction of renewing circulating hemocytes in fatally VP_AHPND-infected prawn was caused by an acute self-destructive immune response by hematopoietic cells.

在甲壳动物中，血细胞是甲壳动物对病原体的先天免疫力的重要组成部分。传染病期间急剧的血红细胞减少显然与疾病的严重程度有关，需要进行健康状况评估和水产养殖管理。用罗氏沼虾攻击的VP _AHPND阐明细菌感染期间血细胞丢失的分子机理。我们在这里报告的血细胞损失与垂死的罗氏沼虾的造血组织的致病性和积极的免疫反应之间的相关性。在这项研究中，给成年淡水虾LC ₅₀剂量的VP _AHPND; 随后细菌清除，并在24小时内达到成功。血细胞存活率增加，而垂死虾的血细胞却急剧减少。垂死虾的造血组织的病理学分析显示出明显的异常体征，包括细菌的存在，少量的有丝分裂细胞，细胞肿胀，结缔组织的松弛和核仁核细胞。在垂死虾的造血组织中检测到核心凋亡机制基因caspase-3的显着上调，但在大肠杆菌DH5α（非致病菌）和VP _AHPND的造血组织中未检测到_上调生存虾。在垂死组中发现最高水平，这证实了该造血组织中细胞凋亡的发生。此外，我们的结果表明造血组织损伤可能是由积极的免疫反应触发的炎症引起的。通过比较对照组，大肠杆菌（DH5α）感染（非致病性）和VP _AHPND感染濒死虾的存活组之间的免疫相关基因表达来表明免疫激活。RT-PCR显示造血组织和血细胞中所有基因在6-12小时内显着上调，到24小时下降。这与几乎VP _AHPND有关的_证据是生存率和大肠杆菌的清除率在垂死组中测定了（DH5α）攻击组与急剧高表达的对比。我们得出结论，致命的VP _AHPND感染的虾中更新的循环血细胞减少是由造血细胞的急性自毁性免疫反应引起的。