Neutrophil immunometabolism in ACLF and sepsis: mechanisms, dysfunction, and therapeutic opportunities
By
Sonali Mukherjee
Takhellambam Malemnganba
Pragyan Acharya
May 22, 2026
Clinical Scorecard: Metabolic Changes in Neutrophils During ACLF and Sepsis: Insights into Mechanisms, Dysfunction, and Potential Treatments
At a Glance
Category Detail
Condition Key Mechanisms Neutrophil metabolic reprogramming, ROS generation, NET formation (ensure sourced). Target Population Care Setting
Key Highlights
Neutrophils exhibit hyperactivation and functional paralysis in ACLF and sepsis (ensure sourced). Both conditions show glycolysis-driven metabolic reprogramming in neutrophils (ensure sourced). ACLF develops on a background of chronic liver disease, while sepsis arises from an acute insult (ensure sourced). A unified framework linking neutrophil immunometabolism to disease pathogenesis is lacking (ensure sourced). Guideline-Based Recommendations
Diagnosis
Identify systemic inflammation and immune dysregulation in ACLF and sepsis (ensure sourced). Management
Consider targeted therapeutic strategies addressing neutrophil immunometabolism (ensure sourced). Monitoring & Follow-up
Assess neutrophil function and metabolic state in patients with ACLF and sepsis (ensure sourced). Risks
Monitor for excessive inflammation and collateral tissue damage due to prolonged neutrophil activation (ensure sourced). Patient & Prescribing Data
Remove speculative insights unless directly supported.
Clinical Best Practices
Utilize transcriptomic and single-cell studies to understand immune and metabolic states (ensure sourced). Implement precision therapies tailored to individual patient profiles in critical illness (ensure sourced). Related Resources & Content
