Peng Wan, Shi Yu, Li Gao-Fei, He Liang-Ge, Liang Yao-Si, Zhang Yong, Zhou Li-Bin, Lin Hao-Ran, Lu Dan-Qi
State Key Laboratory of Biocontrol, Institute of Aquatic Economic Animals and Guangdong Provincial Key Laboratory for Aquatic Economic Animals, College of Life Sciences, Sun Yat-Sen University, Guangzhou, 510275, China.
CAS Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, 164 West Xingang Road, Guangzhou, 510301, China.
Fish Shellfish Immunol. 2016 Sep;56:388-396. doi: 10.1016/j.fsi.2016.07.017. Epub 2016 Jul 15.
Vibriosis is the most common bacterial diseases and brings great economic loss on aquaculture. Vibrio parahaemolyticus (V. parahaemolyticus), a gram-negative bacterium, has been identified as one main pathogens of Vibriosis. The pathogenic mechanism of V. parahaemolyticus is not entirely clear now. In our study, a model of V. parahaemolyticus infection of green-spotted puffer fish (Tetraodon nigroviridis) was established. T. nigroviridis were injected intraperitoneally (i.p.) with 200 μL of V. parahaemolyticus (8 × 10(10) CFU/mL). V. parahaemolyticus infection caused 64% mortality and infected some organs of T. nigroviridis. Histopathology studies revealed V. parahaemolyticus infection induced tissue structural changes, including adipose hollow space in the liver. Immunohistochemistry showed V. parahaemolyticus were present in infected tissue such as liver, head kidney and spleen. In livers of T. nigroviridis infected by V. parahaemolyticus, the alkaline phosphatases (ALP) activity first gradually increased and then backed to normal level, a trend that was on the contrary to the expression profile of the miR-29b. Quantitative real-time PCR analysis showed that the expression level of TLR1, TLR2, TLR5, TLR9, TLR21, NOD1, NOD2 and IL-6 in response to V. parahaemolyticus infection decreased compared to that of non-infected fish. The establishment of the T. nigroviridis model of V. parahaemolyticus infection further confirmed V. parahaemolyticus spreads through the blood circulation system primary as an extracellular pathogen. Meanwhile, liver is an important target organ when infected by V. parahaemolyticus. miR-29b in liver was involved in the progress of liver steatosis during V. parahaemolyticus infection. Moreover, V. parahaemolyticus infection in vivo may have an effect of immunosuppression on host.
弧菌病是最常见的细菌性疾病，给水产养殖业带来巨大经济损失。副溶血性弧菌是一种革兰氏阴性菌，已被确认为弧菌病的主要病原体之一。目前副溶血性弧菌的致病机制尚不完全清楚。在我们的研究中，建立了副溶血性弧菌感染绿斑河豚的模型。给绿斑河豚腹腔注射200μL副溶血性弧菌（8×10¹⁰CFU/mL）。副溶血性弧菌感染导致64%的死亡率，并感染了绿斑河豚的一些器官。组织病理学研究显示，副溶血性弧菌感染引起组织结构变化，包括肝脏中的脂肪空洞。免疫组织化学显示副溶血性弧菌存在于肝脏、头肾和脾脏等感染组织中。在副溶血性弧菌感染的绿斑河豚肝脏中，碱性磷酸酶（ALP）活性先逐渐升高，然后恢复到正常水平，这一趋势与miR-29b的表达谱相反。定量实时PCR分析表明，与未感染的鱼相比，副溶血性弧菌感染后，TLR1、TLR2、TLR5、TLR9、TLR21、NOD1、NOD2和IL-6的表达水平降低。副溶血性弧菌感染绿斑河豚模型的建立进一步证实，副溶血性弧菌主要作为一种细胞外病原体通过血液循环系统传播。同时，肝脏是副溶血性弧菌感染时的重要靶器官。肝脏中的miR-29b参与了副溶血性弧菌感染期间肝脏脂肪变性的进程。此外，副溶血性弧菌的体内感染可能对宿主有免疫抑制作用。
