We found a critical role of IL-1β in the pathogenesis of AAGL model through recruiting T cells to liver, which highlighted that IL-1β antibody might be a candidate therapy for ALF.
In this study, our findings showed that ACD treatment could reduce the high lethality rate; decrease the serum levels of alanine transaminase (ALT), aspartate aminotransferase (AST), monocyte chemoattractant protein (MCP)-1, interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α), and ameliorate the pathological hepatic damage of ALF.
Experimental studies demonstrate that deletion of genes coding for TNF-alpha or IL-1 leads to attenuation of the CNS consequences of ALF and administration of the TNF-alpha receptor antagonist etanercept has comparable beneficial effects in experimental ALF.