Integrated transcriptomic and metabolomic analyses reveal immune-metabolic regulatory mechanisms of Coelomactra antiquata in response to Vibrio harveyi infection.

Coelomactra antiquata is an economically valuable marine cultured bivalve, and its sustainable aquaculture is severely restricted by frequent Vibrio harveyi infection. In this study, optimal infection dosage was screened via mortality statistics, and dynamic changes in physiological-biochemical indices, histopathological lesions, transcriptomic and metabolomic profiles in hepatopancreas were comprehensively investigated between PBS control group (PC) and 1 × 109 CFU/mL V. harveyi infected group (V3) at sequential time points post infection. Physiological results showed that the activities of SOD, CAT and LZM increased firstly and then decreased, reaching the peak at 48 h, while MDA content rose persistently throughout the infection period. AKP and ACP activities displayed obvious time dependent variation patterns after bacterial challenge. Gradually aggravated hepatopancreatic tissue damage was observed, including cell swelling, vacuolation, hemocyte infiltration and digestive tubule structural destruction with prolonged infection duration. A total of 5915 differentially expressed genes (DEGs) were identified in multiple comparison groups. Key immune and stress-related genes such as TLR2, MAPK10, Chac1 and Sod3 exhibited remarkable expression alterations. Functional enrichment revealed that these DEGs were predominantly enriched in innate immune pathway, oxidative stress response, lysosomal function and lipid metabolism processes. Metabolomic analysis identified 346 differential metabolites (most downregulated), demonstrating global metabolic suppression. Metabolic disturbances displayed obvious temporal patterns: lipid metabolites and betaine fluctuated at the early stage linked to membrane injury and osmoregulation, while amino acid derivatives and signal molecules were altered in the middle and late stages. In conclusion, V. harveyi infection triggers oxidative stress, hepatopancreatic damage, innate immune activation and dramatic changes in core genes and metabolites, causing immune disorder and metabolic reprogramming. This study reveals its response mechanisms and offers theoretical support for disease prevention in C. antiquata.