Vibrio parahaemolyticus AHPND infection altered eicosanoid biosynthesis in the gastrointestinal tract of Litopenaeus vannamei.

Acute Hepatopancreatic Necrosis Disease (AHPND) is one of the main culprits for massive shrimp mortality in the aquaculture industry. AHPND is caused by Vibrio parahaemolyticus (VPAHPND) containing plasmids for the PirA and PirB binary toxins. These toxins cause sloughing and cell death in the hepatopancreatic tubules as well as inflammation in the shrimp gastrointestinal tract. Nevertheless, changes in the pro- and anti-inflammatory signaling molecules have yet to be reported. Here, we examined changes in eicosanoid biosynthesis in the Litopenaeus vannamei gastrointestinal tract infected with VPAHPND isolate 5HP. At 24 h post-infection, cyclooxygenase enzyme levels increased in the hepatopancreases of VPAHPND-infected shrimp. The transcription levels of cytosolic phospholipase A2 were elevated in the intestines of VPAHPND-infected shrimp compared with control shrimp. Although the eicosanoid and PUFA profiles were differentially altered in shrimp hepatopancreas, stomach, and intestines, the levels of prostaglandin F2α were elevated, whereas the levels of 5-hydroxyeicosapentaenoic acid and 5-hydroxyeicosatetraenoic acid were suppressed in all three organs of VPAHPND-infected shrimp. These findings suggest that eicosanoid changes may serve as biomarkers for shrimp gastrointestinal health. Moreover, they indicate the conserved nature of the eicosanoid biosynthesis pathway in the host-pathogen response to bacterial infection in crustaceans.