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降低海水盐度可调节免疫反应并提高巨石斑鱼在感染神经坏死病毒后的存活率。

Decreasing salinity of seawater moderates immune response and increases survival rate of giant groupers post betanodavirus infection.

作者信息

Chen Tz-Shiang, Wu Yu-Chi, Chi Shau-Chi

机构信息

Department of Life Science, National Taiwan University, Taipei 10617, Taiwan.

Department of Life Science, National Taiwan University, Taipei 10617, Taiwan; Institute of Molecular Medicine, National Taiwan University, Taipei 10002, Taiwan.

出版信息

Fish Shellfish Immunol. 2016 Oct;57:325-334. doi: 10.1016/j.fsi.2016.08.050. Epub 2016 Aug 26.

DOI:10.1016/j.fsi.2016.08.050
PMID:27569983
Abstract

Giant groupers (Epinephelus lanceolatus), an important aquaculture fish in Asia, are attacked by nervous necrosis virus (NNV), belonging to betanodavirus. Environmental salinity can affect fish immunity and physiology. We examined whether decreasing salinity from 30 to 15 ppt during acclimation of groupers could affect survival with NNV infection and the associated factors. Although NNV infection decreased muscle moisture, up-regulated the gene expression of Na(+)-K(+)-2Cl(-) cotransporter isoform 2, and elevated plasma cortisol level in groupers, these factors were not related to the higher mortality of groupers reared at 30-ppt salinity (S30-groupers), compared to 15-ppt reared groupers (S15-groupers). Infected S30-groupers exhibited high leukocyte count and innate immune gene expression level. Moreover, NNV-infected dead S30-groupers showed high IL-1β gene expression level but low NNV load in the brain. The high or excess IL-1β gene expression levels in the brain of NNV-infected S30-groupers may be the factor in high mortality.

摘要

波纹唇鱼(Epinephelus lanceolatus)是亚洲一种重要的水产养殖鱼类,易受到属于β-诺达病毒的神经坏死病毒(NNV)的攻击。环境盐度会影响鱼类的免疫力和生理机能。我们研究了在波纹唇鱼驯化过程中,盐度从30ppt降至15ppt是否会影响其感染NNV后的存活率及相关因素。尽管NNV感染降低了波纹唇鱼的肌肉水分含量,上调了Na(+)-K(+)-2Cl(-)共转运体亚型2的基因表达,并提高了血浆皮质醇水平,但与饲养在15ppt盐度的波纹唇鱼(S15-波纹唇鱼)相比,这些因素与饲养在30ppt盐度的波纹唇鱼(S30-波纹唇鱼)较高的死亡率并无关联。受感染的S30-波纹唇鱼表现出白细胞计数和先天免疫基因表达水平较高。此外,NNV感染致死的S30-波纹唇鱼大脑中IL-1β基因表达水平较高,但NNV载量较低。NNV感染的S30-波纹唇鱼大脑中IL-1β基因表达水平过高可能是导致高死亡率的因素。

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