Comparative transcriptomic analysis of hepatopancreas reveals that more genes are involved in the exposure response of Vibrio parahaemolyticus PirA compared to PirB.

Vibrio parahaemolyticus (VP-) is regarded as one of the main pathogens that caused acute hepatopancreatic necrosis disease (AHPND) in the Pacific white shrimp Litopenaeus vannamei. PirA and PirB toxin proteins are the main pathogenic proteins of AHPND in shrimp. Knowledge about the mechanism of shrimp response to PirA or PirB toxin is very helpful for developing new prevention and control strategy of AHPND in shrimp. In this study, the pathological sections showed that after 4 h treatment, significant pathological changes were observed in the PirB treated group, and no obvious pathological changes was found in PirA treated group. In order to learn the mechanism of shrimp response to PirA and PirB, comparative transcriptome was applied to analyze the different expressions of genes in the hepatopancreas of shrimp after treatment with PirA or PirB. A total of 9978 differentially expressed genes (DEGs) were identified between PirA or PirB-treated and PBS control shrimp, including 6616 DEGs in the PirA treated group and 3362 DEGs in the PirB treated group. There were 2263 DEGs that were commonly expressed, 4353 DEGs were only expressed in PirA VS PBS group and 1099 DEGs were uniquely expressed in PirB VS PBS group. Among these DEGs, the anti-apoptosis related pathways and immune response related genes significantly expressed in the commonly expressed DEGs of PirA VS PBS group and PirB VS PBS group, and small GTPase-mediated signaling and DNA metabolic process might relate to the host special reaction towards PirA and PirB exposure. The data suggested that the differential expression of these immune and metabolic-related genes in hepatopancreas might contribute to the pathogenicity variations of shrimp to VP-. The identified genes in this study will be useful for clarifying the response mechanism of shrimp toward different toxins of VP- and will further provide molecular basis for understanding the pathogenic mechanism of VP-.