Bovine serum albumin sensitizes the mouse brain to lipopolysaccharides.

This study examined the role of bovine serum albumin (BSA) in lipopolysaccharide (LPS)-induced brain injury. Mice were intraperitoneally injected with either LPS or LPS coupled with BSA. Brain tissues were analyzed for autofluorescence, vascular cell permeability, blood-brain barrier integrity, and pyroptosis. Co-immunoprecipitation and immunostaining were performed to assess the interaction between albumin and LPS. The results showed that, compared to the 5 mg/kg LPS group, the 5 mg/kg BSA-LPS group exhibited enhanced autofluorescence and an increased number of cells with co-localization of propidium iodide (PI) with cluster of differentiation 31 (CD31) and CD13. However, no significant differences were observed between the 25 mg/kg LPS and 25 mg/kg BSA-LPS groups. Horseradish peroxidase (HRP) labeling revealed higher HRP leakage in the 5 mg/kg BSA-LPS group compared to the 5 mg/kg LPS group, a difference that disappeared at the 25 mg/kg dose. Peroxidase staining showed a similar trend. Immunostaining for gasdermin D and CD11b showed significant differences only between the 5 mg/kg LPS and 5 mg/kg BSA-LPS groups. CD68 immunostaining exhibited a similar trend. Furthermore, the study confirmed that albumin binds to LPS in the brain, with more abundant Lipid A+ signals detected in the 5 mg/kg BSA-LPS group compared to the 5 mg/kg LPS group. These findings collectively suggest that albumin boosts the effect of LPS in the brain, probably by binding with LPS and increasing its entry into the brain parenchyma.