Immunometabolic Reprogramming in Experimental Sepsis: A Driver of Multiple Organ Dysfunction Syndrome

Sepsis is a life-threatening syndrome characterized by infection-induced systemic inflammation and immune dysregulation, commonly resulting in the development of multiple organ dysfunction syndrome (MODS), a leading cause of mortality in clinical practice. In decades, immunometabolic reprogramming has been identified as a critical mechanism that contributes to the progression of sepsis and the associated organ injuries. The review provides a systematic overview of the metabolic alterations in immune cells and organs in experimental models of sepsis. Key features include enhanced glycolysis, impaired mitochondrial function, and disturbed lipid metabolism, all of which are closely associated with organ damage. These metabolic adaptations influence immune responses and cell fate decisions, inter-organ crosstalk, and the development of MODS. A detailed examination is conducted on the temporal progression of pathological changes in established animal models, along with organ-specific metabolic dysfunctions and novel therapeutic targets. It emphasizes the importance of dynamic immunometabolic regulation, tissue-specific responses, and inter-organ interactions in the context of sepsis treatment. The integration of multi-omics technologies, identification of reliable biomarkers, and the development of personalized therapeutic strategies should be used to facilitate clinical translation of mechanistic insights.