Yufei Liu, Jinhua Gao, Yuxun Zhang, Gazahegn Wakjira Yadata, Jinliang Zhao
Previous studies on artificial diet domestication in mandarin fish (Siniperca chuatsi) have mainly focused on feeding adaptation, digestive physiology, and basal metabolic regulation. However, whether artificial diet feeding modifies host responses to bacterial infection remains unclear. In this study, Aeromonas hydrophila was used as a bacterial challenge model to compare the responses of mandarin fish fed live bait or an artificial diet. Four groups were established: L, live bait-fed control; AL, live bait-fed infected; A, artificial diet-fed control; and AA, artificial diet-fed infected. Compared with their corresponding controls, both AL and AA showed increased lymphocyte-related indices, reduced neutrophil counts, elevated serum immune-antioxidant indices, and hepatic inflammatory cell infiltration. Compared with A, AA showed significant reductions in red blood cell percentage, mean corpuscular volume, and mean corpuscular hemoglobin. Histological observations further revealed indistinct hepatocyte boundaries and loosely arranged cytoplasm in AA compared with AL. Gene expression analysis showed that interleukin-1β was upregulated, whereas apolipoprotein B and interleukin-8 were downregulated in AA compared with A. Metabolomic analysis identified more differential metabolites in AA vs A (893) than in AL vs L (208). Shared differential metabolites were mainly enriched in nucleotide metabolism, pyrimidine metabolism, the pentose phosphate pathway, and glycerophospholipid metabolism. Metabolites specific to AL vs L were associated with amino acid metabolism, glutathione metabolism, and ABC transporters, whereas those specific to AA vs A were enriched in nucleotide metabolism, one-carbon metabolism, cofactor biosynthesis, and steroid hormone biosynthesis. Collectively, these findings demonstrate that mandarin fish fed different diets exhibit distinct immunophysiological and metabolic responses to A. hydrophila infection, with AA showing more pronounced hepatic injury and broader metabolic remodeling.