ニワトリの斑紋肝臓病における感染動態と宿主バイオマーカーの同定

Spotty liver disease (SLD), primarily caused by Campylobacter hepaticus and (less frequently) by Campylobacter bilis, significantly impacts commercial layer hens by causing liver lesions, reducing egg production, and increasing mortality, meaning it can result in serious economic losses for farmers. This study explored the relationship between infection, liver dysfunction, and reproduction, aiming to identify host genetic markers for tracking SLD progression. Hens were orally inoculated with the C. hepaticus strain NSW44L and monitored over a seven-day period. Pathogen colonisation was quantified using qPCR across the liver, bile, caeca, spleen, and ovarian follicles, while liver lesions were scored and hepatic transcriptomes analysed using RNA-seq. C. hepaticus was detected in the liver, caeca, and spleen from one day post-inoculation (dpi) (1.44-1.68 log₁₀ CFU/mL), appeared in bile by the third dpi (3.64 log₁₀ CFU/mL), and reached the follicles by the fourth dpi (3.25 log₁₀ CFU/mL). The highest bacterial loads were found in bile on days six and seven (up to 7.18 CFU/mL). Liver lesions were first observed on the fourth dpi, reaching their peak at the sixth and seventh dpi. Gene expression analysis in liver tissue revealed a notable downregulation of yolk-precursor and metabolic genes, such as prolactin receptor (PRLR), 7-dehydrocholesterol reductase (DHCR7), and malic enzyme 1 (ME1). In contrast, from days three to seven post-infection, there was significant upregulation of avidin (AVD), a biotin-binding protein, and versican (VCAN), which is linked to tissue remodelling and inflammation. These findings correlate with the disease's progression from initial liver infection to widespread bacterial presence, suggesting value as host biomarkers for effective SLD monitoring and the development of targeted therapies.