Integrated transcriptome and metabolome reveal Mycoplasma hyopneumoniae -induced lipid accumulation, inflammation, oxidative stress, and energy imbalance in the liver of pigs.

Mycoplasma hyopneumoniae (Mhp), the causative agent of swine enzootic pneumonia, has been linked to hepatic dysfunction, however, the underlying metabolic mechanisms remain unclear. We established an Mhp infection model and investigated hepatic responses by integrating transcriptomic and metabolomic analyses. Liver dysfunction was evaluated histologically via H&E staining and serum biochemistry. Mhp infection caused hepatic injury characterized by elevated serum aspartate aminotransferase (AST), triglyceride (TG) accumulation, increased non-esterified fatty acids (NEFAs), and neutrophil infiltration. A total of 3,241 differentially expressed genes and 685 metabolites were identified and were enriched in PPAR signaling, inflammatory, and energy metabolism pathways. Genes related to fatty acid oxidation, antioxidation, and energy metabolism were downregulated, whereas those associated with TG synthesis and inflammation were upregulated. Reduced cyclic adenosine monophosphate (cAMP) levels, decreased superoxide dismutase (SOD) activity, and elevated hydrogen peroxide (H2O2) and malondialdehyde (MDA) indicated oxidative stress and impaired energy production. These findings provide mechanistic insights into Mhp-induced hepatic metabolic injury and potential therapeutic targets.