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• W2309826094 abstract "Introduction Activation of systemic inflammatory responses in acetaminophen-induced acute liver failure (AALF) is associated with elevated levels of both pro- and anti-inflammatory cytokines. Functional monocyte deactivation has been described and this is thought to contribute to increased susceptibility to sepsis and a higher mortality rate. Anti-inflammatory cytokines play a major part in the resolution of inflammatory responses and promote tissue repair processes but increase the risk of systemic infections. We hypothesise that the levels of anti-inflammatory cytokines mirror the severity of hepatic necrosis and reflect attempts to resolve inflammation during AALF. It is the excessive production of these mediators that “spill-over” and increase the risk of systemic sepsis. We sought to delineate hepatic and systemic cytokine responses in experimental and human AALF, and, determine whether there is production of anti-inflammatory cytokines in the liver which “spill-over” into the systemic circulatory compartment. Aim We sought to delineate hepatic and systemic inflammatory responses in experimental and human AALF, and, determine whether there is a “spill-over” of hepatic anti-inflammatory mediators into the systemic, circulatory, compartment. Method Median levels (pg/ml) of hepatic IL-1s, IL-4,-6,-10,-12,-17, IFN-Y, MCP-1, TNF-α, TGF-s1 were measured using proteome arrays in 10 human AALF explants and 8 normal control liver tissue samples. Hepatic and serum levels of IL-1s, IL-4,-6,-10,-12,-17, MCP-1, TNF-α, TGF-s1 were measured in 200mg/kg i.p. APAP treated male C3H/HeH mice (n=5 severe necrosis, n=5 moderate necrosis) and 5 control mice. Regional levels (portal vein (PV)), hepatic vein (HV), arterial (art)) of TNF-α, IL-10 were determined using ELISA in 3 AALF patients at time of liver transplantation. Results In human AALF, hepatic levels of IL-6 (115 vs 75; p=0.02), IL-10 (1.8 vs 0.6; p=0.03), TGF-s1 (3009 vs 1323; p Conclusion We demonstrate a hepatic inflammatory microenvironment favouring resolution of inflammation/tissue repair processes. In vivo hepatic production and systemic “spill-over” of the immunosupressive cytokines is observed and may account for functional monocyte deactivation and the marked predisposition to sepsis in AALF. The marked similarities in anti-inflammatory mediator profiles between human and murine models of AALF provide a rationale on which to base the studies examining evolution of disease and development of immunomodulatory strategies to ameliorate acute liver injury and promote tissue repair." @default.
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• W2309826094 date "2010-09-01" @default.
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• W2309826094 title "P100 Intrahepatic and system cytokine profiles in acetaminophen-induced acute liver failure: possible mechanism of immuneparesis" @default.
• W2309826094 doi "https://doi.org/10.1136/gut.2010.223362.126" @default.
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