To summarize the roles of neutrophil functional dysregulation and newly identified functional subsets in the pathogenesis of sepsis, and to analyze the molecular regulatory mechanisms of different death modes.
Key Findings:
Neutrophils exhibit aberrant activation and prolonged lifespan due to the upregulation of anti-apoptotic proteins.
Excessive neutrophil accumulation can lead to fatal inflammatory responses and organ damage.
Newly identified neutrophil subsets have unique functions that contribute to sepsis progression.
Interpretation:
Neutrophil dysfunction plays a critical role in the pathophysiology of sepsis, influencing both immune responses and disease outcomes.
Limitations:
The review may not cover all potential neutrophil functions and interactions in sepsis.
Further research is needed to fully elucidate the mechanisms underlying neutrophil dysregulation.
Conclusion:
Targeting neutrophil function and programmed cell death presents a promising therapeutic strategy for improving outcomes in sepsis.
Phase 3 ENHANCE-1 results showed higher composite clinical cure and microbiologic response rates with cefepime-zidebactam vs meropenem in hospitalized adults with complicated urinary tract infection or acute pyelonephritis.
