A dual role of inflammation in acetaminophen-induced liver injury

Abstract

In many affluent nations, acetaminophen (APAP) overdose is the leading cause of drug-induced acute liver failure. The process of APAP-induced liver injury (AILI) is intimately tied to inflammation, including hepatocyte necrosis-caused initiation of inflammation, inflammation amplification that exacerbates liver injury, and the resolution of inflammation that triggers liver regeneration and repair. Excessive APAP metabolism in the liver eventually leads to hepatocyte necrosis and inflammation. Innate immune cells, such as neutrophils, eosinophils, monocytes, and gammadelta T cells, are recruited into the injured liver and release various cytokines. These immune cells and cytokines have been found to serve two purposes in AILI. In this review, we highlighted the dual role of inflammation, including inflammatory cytokines and inflammatory immune cells in AILI, and discussed possible explanations for contradictory findings.

Keywords

• Acetaminophen (APAP)
• Acute liver failure
• Acetaminophen-induced liver injury (AILI)
• Inflammation
• Immune mechanism