Hepatic transcriptomics reveals immuno-metabolic interactions in juvenile channel catfish (Ictalurus punctatus) after...

In aquaculture, disease outbreaks occur amidst complex husbandry factors like feeding schedule and incidental injury. The liver, a central immunometabolic organ, integrates these cues, but the systems-level transcriptional mechanisms governing its response to concurrent stress are poorly defined in channel catfish. We investigated how feeding status and physical injury modulate the hepatic transcriptome during early Aeromonas hydrophila infection in channel catfish.

Juvenile channel catfish were assigned to four treatment groups reflecting combinations of feeding status (fed or fasted) with or without adipose fin‑clipping followed by immersion challenge with virulent A. hydrophila. Although the design captured interactions among these factors within the infected groups, it does not represent a full factorial structure as all infected groups were only compared to (fed with or without fin-clipping controls) and did not include the reciprocal (fasted with or without fin-clipping controls). Histopathology at 2, 4, and 8 h post-challenge (hpc) revealed progressive vascular congestion and immune infiltration primarily in fasted, unclipped fish. RNA-Seq analysis of liver tissue, focusing on genes that were differentially expressed across all timepoints when compared to fed with or without fin-clipping controls, showed marked transcriptional reprogramming. Under the present experimental and control framework, fasted fish showed a stronger stress-adaptive signature, including downregulation of genes in acyl-CoA biosynthesis (tecrb, hacd2, acsl2) and the TCA cycle (idh2, aco2), alongside strong upregulation of cytokine networks (il1β, cxcl18b). This coincided with KEGG pathway enrichment for fatty acid elongation, steroid biosynthesis, and PPAR signaling. In contrast, fed fish maintained hepatic architecture and showed a more restrained immune response, with enriched oxidoreductase activity in sterol metabolism (dhcr24, dhcr7, tm7sf2), though these anabolic pathways were also suppressed. Fin-clipping was associated with greater pro-inflammatory signaling, but these patterns should be interpreted in the context of the relevant sham control structure.

Our findings suggest that feeding status shapes the early hepatic response during septicemia. Short-term fasting appears to prime the liver for a catabolic, stress-responsive state that may compromise metabolic resilience, while feeding supports homeostasis when compared to fed clipped or unclipped controls. This provides a rationale for nutritional management as an important strategy to enhance metabolic readiness and disease resilience in aquaculture, offering novel targets for functional genomics studies in fish health.