Bo Liu
Chongqing Medical University, China
Title: Regulation of metabolic reprogramming in alveolar macrophages alleviates lipopolysaccgaride-induced acute respiratory distress syndrome
Biography
Biography: Bo Liu
Abstract
Introduction: Acute Respiratory Distress Syndrome (ARDS) is a common clinical critical illness with a high mortality rate and currently lacks effective prevention and treatment measures. Imbalance in alveolar macrophage polarization plays a crucial role in the occurrence and development of ARDS, but the specific mechanisms underlying alveolar macrophage polarization are still unclear.
Methods: In vivo experiments were conducted using intratracheal administration of LPS to establish an ARDS mouse model, while in vitro experiments utilized LPS-induced MH-S mouse alveolar macrophages to observe changes in metabolism and phenotype during ARDS. The therapeutic effects of the addition of the glycolysis inhibitor 2-DG were observed and the specific mechanisms were explored.
Results: In LPS-induced ARDS mice, significant inflammatory responses and lung tissue damage were observed, accompanied by an increase in glycolysis levels. The addition of 2-DG markedly alleviated LPS-induced lung injury and reduced inflammation. Mechanistically, LPS induction increased glycolysis levels in alveolar macrophages, promoting polarization towards the M1 pro-inflammatory phenotype. Inhibiting glycolysis shifted alveolar macrophages from the M1 pro-inflammatory phenotype to the M2 anti-inflammatory phenotype .
Conclusions: Metabolic reprogramming, represented by glycolysis, plays a significant role in alveolar macrophage polarization and modulating the metabolism of alveolar macrophages may be a potential therapeutic approach for ARDS.