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The liver is a crucial organ responsible for cytokine production and storage. In instances of acute liver injury, tissue cells are afflicted by multiple cytokines operating in conjunction and leading to inflammation. Researchers have analyzed changes in the levels of various cytokines in human subjects before the onset of liver injury and found that elevated levels of IL-1β, IL-10, IL-12, IL-13, and TNF-α precede the escalation of serum liver enzyme levels. This study proposes certain cytokines or related molecules as early biomarkers of liver injury. The selection of cytokines for therapeutic drug targeting may aid in the development of treatments for liver injury because cytokines are non-invasive, easy to detect, and reflect the biological process of liver injury.
ALF is a severe clinical syndrome caused by massive necrosis of hepatocytes due to various factors such as virus, immunity, and metabolism. Recent studies have established Kupffer cells (KC) activation in the liver as the pivotal event in ALF pathogenesis. The cytokines released by KCs encode the inflammatory response at the hepatic injury site, and their involvement accelerates and exacerbates the necrotic process, leading to hepatocyte death. IL-18 levels were significantly increased in patients with acute hepatitis. Additionally, IFN-γ is known to play a crucial role in the mechanism underlying acute hepatocellular injury.
DILI is a common adverse drug reaction involving liver damage caused by the drug or its metabolites during drug administration. Previous experimental studies suggest that IL-17 may contribute significantly to DILI, particularly immune-mediated liver damage. Moreover, IL-10, a cytokine that offers protection, can suppress the immune response and the production of various pro-inflammatory cytokines, potentially mitigating the extent of liver damage. Relevant studies have demonstrated the involvement of IL-10 in several immune-mediated liver diseases, including DILI.
Figure 1. Mechanisms of immunity in DILI. (Liu W, et al., 2021)
HIRI is a phenomenon that may occur after a period of hepatic tissue ischemia following severe, traumatic liver surgery or liver transplantation during which blood flow is temporarily restored, and the resulting injury is aggravated. Tissue ischemia hastens the liberation of cytokines and other inflammatory markers, resulting in the blockage of hepatic microcirculation vessels. TNF-α is believed to play a pivotal role in the progression of HIRI, and its possible mechanism involves controlling the creation of lipid and peptide mediators that contribute to inflammation and tissue damage. Moreover, augmented IL-6 expression was ascertained in HIRI resulting from liver transplantation. With an increase in the expression of IL-6, there was a gradual reduction in TNF-α production. This suggests that IL-6 effectively controls the inflammatory response during HIRI, indicating its protective effect on the liver by reducing TNF-α.
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