Integrated transcriptomic and metabolomic analyses reveal host-metabolite interactions underlying cloacal inflammation in laying Pekin ducks.

Abstract

Objective: Cloacal inflammation in laying ducks, often accompanied by prolapse, is a major threat to animal welfare, productivity, and intestinal health. However, the underlying molecular and metabolic mechanisms remain largely unclear.

Methods: Cloacal tissues and contents from inflamed and healthy laying Pekin ducks were examined histologically, transcriptomically, and metabolomically. Cross-omics integration was used to identify coordinated molecular and metabolic changes.

Results: Hematoxylin and eosin staining showed a loose and disorganized structure of the cloacal sphincter in inflamed ducks. Transcriptomic analysis identified differentially expressed genes that are enriched in immune signaling, inflammatory response, and epithelial repair pathways. Metabolomic profiling revealed significant alterations in taurine- and lipid-related metabolic pathways. Integrated analysis highlighted coordinated changes between immune-related genes (COL6A3, SPARC, PPEF1, HSD17B2, and KCNG2) and key metabolites including Hydroxytyrosol-Ac, Phytol, GG-alcohol, MeCys-SO, Thiazoline, and PEA-glu.

Conclusion: The findings provide a multi-omics perspective on cloacal inflammation in laying Pekin ducks, highlighting host-metabolite interactions that may play a role in immune activation and epithelial barrier dysfunction.