Integrated multi-omics analysis identifies PPAR signaling network associations with metabolic-immune dysregulation and intestinal injury in PDCoV-infected piglets

Metabolomic analysis demonstrated widespread degradation of membrane glycerophospholipids and alterations in the arachidonic acid–prostaglandin inflammatory axis, as evidenced by substrate consumption and accumulation of the pro-inflammatory mediator 20-hydroxy-PGE2. We propose a hypothetical working model in which PDCoV infection is associated with PPAR network modulation, potentially contributing to lipid resource reallocation and the establishment of a pro-inflammatory microenvironment that may exacerbate intestinal injury.

Notably, similarities can be observed between these PDCoV-associated alterations and the metabolic-immune dysregulation reported in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, raising the hypothesis of shared pathogenic features across coronaviruses. Our findings highlight the PPAR pathway and its downstream lipid mediators as potential therapeutic targets warranting further investigation, and suggest that existing PPAR agonists may merit evaluation as candidate drugs for repurposing in future studies.</p>