Gut microbiota dysbiosis in sepsis and sepsis-associated organ injury: mechanisms, gut-organ axes, and therapeutic strategies.

Sepsis is a life-threatening syndrome caused by a dysregulated host response to infection and remains a major cause of morbidity, mortality, and organ dysfunction worldwide. Gut microbial dysbiosis in sepsis may result from both disease pathophysiology and ICU interventions, including broad-spectrum antibiotics, vasopressors, enteral or parenteral nutrition, mechanical ventilation, renal replacement therapy, immune status, and baseline comorbidities. Increasing evidence suggests that gut microbial dysbiosis is closely associated with sepsis progression and sepsis-associated organ injury, and may act as both a consequence of critical illness and a potential contributor to disease progression in selected experimental and clinical contexts. Host-microbe interactions, microbial metabolites, and immune-metabolic signaling help explain how gut dysbiosis contributes to sepsis pathophysiology. At the same time, probiotics, fecal microbiota transplantation, and selected microbial metabolites have shown possible benefits, mainly in experimental or selected clinical settings. This review integrates gut dysbiosis, microbial product translocation, microbial metabolites, and host-microbe interactions into a gut-organ axis framework, and evaluates how these mechanisms may contribute to sepsis progression, organ injury, and microbiota-targeted therapeutic strategies.