Short-Chain Fatty Acids: A Key Modulator of Sepsis-Associated Acute Respiratory Distress Syndrome

Area of Science:

• Microbiology
• Immunology
• Pulmonology

Background:

• Sepsis-associated acute respiratory distress syndrome (ARDS) is a fatal complication.
• Intestinal flora imbalance is a key factor in ARDS pathogenesis.
• Microbial translocation, inflammation, and immune dysregulation link gut dysbiosis to lung injury.

Purpose of the Study:

• To review the mechanisms of ARDS caused by intestinal flora imbalance.
• To explore the bidirectional regulatory properties of short-chain fatty acids (SCFAs).
• To discuss intestinal flora-based intervention strategies for sepsis-associated ARDS.

Main Methods:

• Systematic review of existing literature.
• Analysis of the role of SCFAs (acetate, propionate, butyrate) in ARDS.
• Examination of SCFA mechanisms involving histone deacetylase (HDACs) and G protein-coupled receptors (GPCRs).

Main Results:

• Intestinal dysbiosis promotes ARDS through microbial translocation, systemic inflammation, and immune dysregulation.
• Depletion of SCFAs accelerates ARDS progression.
• SCFAs exert protective effects via anti-inflammatory, immunomodulatory, and barrier-protective actions.
• SCFAs exhibit concentration, type, and inflammation stage-dependent bidirectional regulatory properties.

Conclusions:

• Understanding the bidirectional regulation of SCFAs is crucial for personalized ARDS therapies.
• Targeting intestinal flora and SCFA metabolism offers novel therapeutic avenues for sepsis-associated ARDS.
• Precision dosing and personalized interventions are key for effective clinical management.