AVANZI Gian Carlo
Research Activity
Brief Research Description
GAS6 regulates the immune response by inhibiting TNF-α and IL-6 secretion in LPS-stimulated monocytes/macrophages. Among GAS6 receptors, only Mer is expressed in differentiated U937 cells, activating a pathway that involves PI3K/Akt/GSK3, leading to reduced cytokine expression. Mer activation following GAS6 stimulation increases Akt phosphorylation and inhibits NF-κB nuclear translocation. This elucidates GAS6's role in modulating macrophage cytokine secretion through an anti-inflammatory pathway.
Investigation on the role of Gas6/Mer and TPO/Mpl axes in severe sepsis and septic shock. These pathways are proposed to be involved in the inflammatory response and organ dysfunction seen in sepsis. Through animal models and human cohorts, we aim to determine if modulating these systems can control disease severity and improve outcomes. Additionally, we seek to identify Gas6, sMer, and TPO plasma concentrations as potential predictors and markers for risk stratification in sepsis. The study promises to advance our understanding of sepsis pathophysiology and may reveal new therapeutic targets and biomarkers.
Keywords
Sepsis – Septic shock – Inflammation – Organ dysfunction – Disease markers