Hypoxia stress priming improves resistance to Vibrio parahaemolyticus in the ridgetail white prawn (Exopalaemon carinicauda): Phenotypic and transcriptomic evidence

This study investigated the relationship between hypoxia stress priming and resistance to Vibrio parahaemolyticus infection in ridgetail white prawns ( Exopalaemon carinicauda ). Females and males were compared between group H (hypoxia‐primed) and group C (control). Four groups—CF, HF, CM, and HM—were infected with an established LC50 dose (1.46 × 10 5 CFU/mL) of V. parahaemolyticus . After 96 h, the survival rate of the hypoxia‐primed groups (HF and HM) exceeded 50%, which was significantly higher than the control groups (CF and CM) (less than 40% survival). Bacterial load analysis revealed significantly higher ( p < 0.01) mean V. parahaemolyticus loads at 96 h in the control groups (CF: 3.97 × 10 5 CFU/mg; CM: 2.71 × 10 5 CFU/mg) compared to the hypoxia‐primed groups (HF: 2.60 × 10 5 CFU/mg; HM: 1.22 × 10 5 CFU/mg), with significant differences persisting at 120 h. The analysis confirmed a significant positive correlation between hypoxia stress priming and resistance to infection, evidenced by a significant negative correlation between hypoxia stress priming and bacterial load in both males ( r = −0.574, p < 0.01) and females ( r = −0.496, p < 0.01). In other words, the hypoxia stress priming corresponded to a lower bacterial load (higher resistance). Transcriptome analysis of hepatopancreatic tissues identified 106 differentially expressed genes (39 up, 67 down) in hypoxia‐primed versus control prawns. The genes were primarily enriched in metabolic pathways (KEGG: beta‐alanine metabolism, metabolic pathways, glycolysis/gluconeogenesis, carbon metabolism, propanoate metabolism) related to functions in cell wall components and carbohydrate/GABA processes (GO: hyphal/fungal‐type cell wall, carbohydrate metabolic process, gamma‐aminobutyric acid catabolic/metabolic processes). The different expression levels of these genes may explain the variation in resistance to V. parahaemolyticus infection linked to hypoxia stress priming.