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Review
. 2020 Oct 19;24(1):614.
doi: 10.1186/s13054-020-03327-1.

Gut-liver crosstalk in sepsis-induced liver injury

Affiliations
Review

Gut-liver crosstalk in sepsis-induced liver injury

Jian Sun et al. Crit Care. .

Abstract

Sepsis is characterized by a dysregulated immune response to infection leading to life-threatening organ dysfunction. Sepsis-induced liver injury is recognized as a powerful independent predictor of mortality in the intensive care unit. During systemic infections, the liver regulates immune defenses via bacterial clearance, production of acute-phase proteins (APPs) and cytokines, and metabolic adaptation to inflammation. Increased levels of inflammatory cytokines and impaired bacterial clearance and disrupted metabolic products can cause gut microbiota dysbiosis and disruption of the intestinal mucosal barrier. Changes in the gut microbiota play crucial roles in liver injury during sepsis. Bacterial translocation and resulting intestinal inflammation lead to a systemic inflammatory response and acute liver injury. The gut-liver crosstalk is a potential target for therapeutic interventions. This review analyzes the underlying mechanisms for the gut-liver crosstalk in sepsis-induced liver injury.

Keywords: Gut-liver crosstalk; Inflammation; Liver injury; Metabolism; Microbiota dysbiosis; Sepsis.

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Conflict of interest statement

No competing interests.

Figures

Fig. 1
Fig. 1
Effect of increased levels of inflammatory cytokines and decreased bacterial clearance in sepsis-induced liver injury on the gut
Fig. 2
Fig. 2
Effect of cytokines on the gut barrier during sepsis. During sepsis, increased levels of cytokines can modulate gut permeability by regulating the protein expression of claudins, JAM-A, occludin, and ZO-1. The phosphorylation of myosin regulatory light chain by myosin light chain kinase (MLCK) can increase paracellular permeability and result in contraction or opening of the apical tight junctions
Fig. 3
Fig. 3
The role of bile acids in the gut-liver axis. During sepsis, the liver receives microbial input and influences intestinal microbes via bile acids. The gut microbiota can contribute to the pathogenesis of sepsis-induced liver injury by altering bile acids metabolism and its signaling pathways

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