Fatty liver hemorrhagic syndrome (FLHS) affecting laying hens represents a metabolic-nutritional condition whose principal manifestations include liver enlargement, lipid accumulation within hepatocytes, and intrahepatic bleeding. This disorder tends to emerge during the phase of maximal egg production, causing substantial financial setbacks for the poultry sector; however, the exact mechanisms driving FLHS remain poorly understood. Investigations conducted by our team, along with earlier reports, have revealed that concentrations of bile acids drop considerably as fatty liver progresses, and that purposeful stimulation of signaling cascades involving bile acids can assist in both averting and managing fatty liver. For the current work, we produced an FLHS model in laying hens by administering a diet rich in energy but low in protein, while supplying goose deoxycholic acid (CDCA) as a therapeutic measure. Hematoxylin-eosin staining, fluorescence-based quantitative PCR, and ELISA techniques were applied to gauge CDCA’s influence on hepatic pathological alterations and inflammatory processes. Outcomes revealed a noticeable reduction in hepatic bleeding among FLHS-affected hens receiving CDCA. Similarly, fatty vacuoles and circulating transaminase enzymes declined markedly. Beyond this, indicators of M1-polarized macrophages and their secretory products were sharply downregulated, and mediators promoting inflammation tied to the JAK-STAT cascade, the LPS-TLR4-Myd88–NF-kB axis, and NLRP3 inflammasome assembly were also substantially diminished. Conversely, markers of M2-polarized macrophages and their associated products rose notably, paralleled by heightened expression of anti-inflammatory components associated with the JAK-STAT pathway. Collectively, these findings indicate that CDCA mitigates hepatic damage in FLHS laying hens by restraining M1-type macrophage polarization and the accompanying pro-inflammatory cascade, while simultaneously encouraging M2-type polarization and an inflammation-resolving response.
