Causal associations of circulating inflammatory proteins with sepsis: a two-sample Mendelian randomization study

Our study elucidates roles of inflammatory mediators in sepsis pathogenesis. The identified proteins may serve as biomarkers or therapeutic targets. TRAIL signaling inhibition may hold promise for future clinical translation given its causal links to increased sepsis risk and mortality. CCL28 and CCL4 also represent potential immunological drivers of sepsis mortality worthy of further investigation. Meanwhile, the neurotrophins beta-NGF and TNFB emerged as having protective effects in sepsis that could be therapeutically augmented. Further experimental validation is warranted to confirm the observed causal relationships. Our findings provide targets for future mechanistic and clinical examination to impact patient prognosis.