Insights into the fatty acid binding protein of Pacific white shrimp (Litopenaeus vannamei) suffering acute hepatopancreatic necrosis disease infection

Abstract

Acute hepatopancreatic necrosis disease (AHPND) has a significant economic impact on aquaculture worldwide. However, the molecular mechanism responsible for AHPND remains unknown. Our previous study demonstrated that the Litopenaeus vannamei fatty acid binding protein (LvFABP) interacted with the Vibrio parahaemolyticus toxin PirB, and that silencing LvFABP using RNA interference improved AHPND resistance in shrimp. Polyclonal antibodies against recombinant LvFABP and PirBvp toxin were produced to further elucidate the role of LvFABP in AHPND resistance. Immunofluorescence localization showed that LvFABP was abundant throughout the cytoplasm of the hepatopancreas cells, and a co-localization assay revealed that PirBvp directly interacted with LvFABP. Antibodies against LvFABP were able to partially block the binding of LvFABP to PirBvpin vitro and inhibited AHPND infection in vivo. Exogenous recombinant LvFABP had a partially neutralizing effect against AHPND and gave L. vannamei significant protection against infection. In addition, recombinant LvFABP treatment of L. vannamei significantly reduced the morphological damage to the shrimp following pathogen challenge. The transcriptomes of the L. vannamei hepatopancreas with and without V. parahaemolyticus infection after silencing of LvFABP by RNA interference were also explored. The results showed that AHPND infection could affect the health of L. vannamei via functional changes in carbohydrate metabolism, lipid metabolism, and transport and catabolism. Furthermore, silencing LvFABP could effectively protect metabolism, transport and catabolic homeostasis, thus enabling adaptation to further or prolonged AHPND infections. These findings provided a unique and important dataset that deepened our understanding of the pathological mechanism of AHPND and may help in the development of strategies to prevent and ameliorate the effects of bacterial diseases.