![]() Upon pathogen infection, the host innate immune system is excessively activated innate immune activation is followed by and causes the occurrence of a cytokine storm, which is characterized by high levels of pro-inflammatory cytokines, including TNF-α, IL-1β, IL-6, and IFN-γ, and results in cell death and multiple organ dysfunction. Sepsis is a common complication after infection, shock and severe trauma, and it is one of the major causes of mortality in patients in intensive care units (ICUs). ![]() In summary, our findings demonstrate for the first time that S100A9 plays an important pro-inflammatory role in sepsis-mediated ALI by regulating AKT-AMPK-dependent mitochondrial energy metabolism and highlights that targeting S100A9 may be a promising new approach for the prevention and treatment of sepsis-related liver injury. Finally, the administration of the S100A9 inhibitor Paquinimod (Paq) to WT mice protected against CLP-induced mortality, liver injury and mitochondrial dysfunction. In contrast, treatment with the AMPK inhibitor Compound C reversed the inhibitory effects of S100A9 KO on CLP-induced liver dysfunction and injury in vivo. Moreover, S100A9-KO in mice markedly attenuated CLP-induced liver dysfunction and injury, promoting the AMPK/ACC/GLUT4-mediated increases in fatty acid and glucose uptake as well as the improvement in mitochondrial function and ATP production. Our results indicated that S100A8/A9 expression was significantly upregulated in the livers of septic mice 24 h after cecal ligation and a puncture (CLP) operation. However, the role of S100A8/A9 in the regulation of sepsis-induced ALI remains known. ![]() S100A8/A9 is known to promote inflammation and immune responses. ![]() Acute liver injury (ALI) is recognized as a serious complication of sepsis in patients in intensive care units (ICUs). ![]()
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