Seminars

Acute hepatopancreatic necrosis disease (AHPND) caused by Vibrio parahaemolyticus carrying toxin producing plasmid, has led to severe mortalities in farmed Penaeid shrimp throughout Asia. Previous studies have reported that a non-lethal heat shock (NLHS) could enhance disease tolerance in aquatic animals.  In this study, we investigate whether the NLHS could enhance the survival of Pacific white shrimp Litopenaeus vannamei upon challenge with an AHPND-causing strain of V. parahaemolyticus (VPAHPND). Abruptly exposure of juvenile shrimp from 28 oC to 38 oC for 5 min every day for 7 days followed by VPAHPND challenge could enhance shrimp survival over 50% as compared to 20% of the non-heated shrimp control.   The qRT-PCR analysis revealed that the expression of heat shock proteins, LvHSP70, LvHSP90 as well as other immune-related genes, LvproPO and LvCrustin, were induced upon exposure of shrimp to NLHS. Interestingly, gene silencing of LvHSP70 and LvHSP90 eliminated the VPAHPND resistance in the NLHS-treated shrimp and had decreasing PO activity suggesting that these LvHSPs played crucial roles in bacterial defense in shrimp. To further characterize the specific function of LvHSP70, the recombinant protein (rLvHSP70) was produced and injected into the shrimp to observe the protective effect against bacterial infection.  It was found that shrimp receiving rLvHSP70 showed an increased survival rate (75%) to VPAHPND infection compared to 20% survival in the control group injected with bovine serum albumin (BSA). The injected rLvHSP70 accumulated in shrimp hemocytes and induced expression (P<0.05) of several immunerelated genes (LvMyD88, LvIKKβ, LvIKKε, LvCrustinI, LvPEN2, LvPEN3, LvproPO1, LvproPO2 and LvTG1). Collectively, these results suggest that heat shock treatment could enhance disease resistance in shrimp by induction of HSPs that mediate activation of the innate immune system.