Lbp, short for Lipopolysaccharide-binding protein, is a significant protein in the host's innate immune defense. It binds to bacterial lipopolysaccharide (LPS), transfers LPS to its cellular receptor or lipoproteins, and also interacts with other bacterial compounds like lipoteichoic acid (LTA) and lipopeptides, modulating the host's innate immune system [2]. Lbp is synthesized in hepatocytes and secreted into the bloodstream, and its levels rise substantially during the acute-phase response [4].

In a rat sepsis model, deletion of Lbp reduced LPS-induced liver inflammation and injury at 1 and 6 h, but at 24 h, mitochondrial damage and reactive oxygen species (ROS) levels were higher in Lbp-/-rat livers compared to wild-type (WT) rat livers. Lbp protects hepatic mitochondria against LPS-induced damage via the Lbp-PPARα-CYP4a2 signaling pathway [1]. In Trachinotus ovatus, ToBPI1/LBP and ToBPI2/LBP (two BPI/LBPs) were significantly expressed in immune-related tissues after being challenged with bacteria, showing antibacterial activity against certain Gram-negative and Gram-positive bacteria [3]. Also, TroBPI/LBP from Trachinotus ovatus was constitutively expressed in tested tissues, with the highest expression in the liver. Its mRNA expression was upregulated in immune-related tissues after Vibrio alginolyticus stimulation, and overexpression of TroBPI/LBP enhanced the fish's ability to resist V. alginolyticus infection while knockdown diminished bacterial clearance capacity [5].

In conclusion, Lbp plays a crucial role in the innate immune defense against bacterial infections and in protecting hepatocyte mitochondrial function during sepsis. Gene knockout models in rats and fish have revealed its importance in specific biological processes related to inflammation, mitochondrial function, and antibacterial immunity, providing insights into potential therapeutic targets for sepsis and enhancing understanding of host-pathogen interactions.