Hepatic Inflammatory Response to Exogenous LPS Challenge is Exacerbated in Broilers with Fatty Liver Disease

SIMPLE SUMMARY: Fatty liver disease is the most common liver abnormality, characterized by lipid accumulation within the hepatocytes. The disease results in a significant economic burden on the poultry industry. Microbial infection is recognized as a continuous challenge worldwide. The current study evaluated hepatic function and inflammatory response in broilers with fatty livers following acute lipopolysaccharide (LPS) challenge. Results indicate that broilers suffering from fatty liver disease are more susceptible to the negative effects of LPS, showing inflammatory response activation and more severe damage to the liver. ABSTRACT: This study aimed to examine hepatic function and inflammatory response in broilers with fatty livers, following acute lipopolysaccharide (LPS) challenge. One-day-old Lihua yellow broilers were fed a basal diet. Broilers were divided into four groups: control (CON), corticosterone treatment (CORT), LPS treatment (LPS), and LPS and CORT treatment (LPS&CORT). Results show that CORT induced an increase in plasma and liver triglycerides (TGs), which were accompanied by severe hepatic steatosis. The LPS group showed hepatocyte necrosis with inflammatory cell infiltration. Total liver damage score in the LPS&CORT group was significantly higher than that in the LPS group (p < 0.05). Activity levels of plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were similar in the CON and CORT groups, but higher in the LPS group. Gene expression upregulation of the proinflammatory cytokines (NF-κB, IL-1β, IL-6, IFN-γ, and iNOS) was also noted in the LPS group (p < 0.05). In particular, LPS injection exacerbated the gene expression of these proinflammatory cytokines, even when accompanied by CORT injections (p < 0.05). In summary, our results indicate that broilers suffering from fatty liver disease are more susceptible to the negative effects of LPS, showing inflammatory response activation and more severe damages to the liver.