Genetic expression of retinol dehydrogenase 12 and all-trans-retinol 13,14-reductase during acute hepatopancreatic necrosis disease in Penaeus monodon: insight into retinoids metabolism in pathogenesis

Abstract

Vibrio parahaemolyticus (VpAHPND), the bacterium that causes acute hepatopancreatic necrosis disease (AHPND), is a severe hazard to shrimp aquaculture worldwide. Despite substantial research into AHPND pathophysiology, the role of retinoid metabolism in shrimp immunological responses remains unknown. We aimed to investigate the functions of retinol dehydrogenase 12 (RDH12) and all-trans-retinol 13,14-reductase (AT-R 13,14-R) during VpAHPND infection to better understand their contribution to retinoid metabolism and immunological responses in Penaeus monodon. Toward this, hepatopancreatic tissue samples were obtained at different time points (0, 3, 6, 12, 24, 36, and 48 h post-infection (hpi)) from P. monodon infected with VpAHPND (KS17.S5-1 strain). Quantitative real-time PCR (qRT-PCR) analysis of these samples revealed a substantial overexpression of RDH12 (sixfold) in the infected group compared to the control, with a peak expression of 6.11 ± 0.15-fold at 12 hpi. AT-R 13,14-R showed a ninefold downregulation, with the lowest expression of − 9.69 ± 0.04-fold at 3 hpi. These findings suggest that AHPND affects the retinoid signaling system, jeopardizing immune defenses and metabolic control. Thus, restoring this system may reduce the impact of harmful chemicals, leading to new treatment options, such as dietary supplementation with retinoid precursors, to protect shrimp farms against AHPND.