| Summary: | Yuting Sun,1,2 Meilin He,3 Jiaqi Li,1 Chaomin Wu,2 Shuming Pan1 1Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Department of Emergency, Shanghai, 200062, People’s Republic of China; 2Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Department of Respiratory Medicine, Shanghai, 200062, People’s Republic of China; 3School of Basic Medical Sciences Zunyi Medical University, Department of Laboratory Medicine, Zunyi City, 563000, People’s Republic of ChinaCorrespondence: Shuming Pan; Chaomin Wu, Email panshuming1103@163.com; wuchaomin2018@hotmail.comAbstract: Sepsis-associated acute respiratory distress syndrome (ARDS) is a common clinical fatal complication, and intestinal flora imbalance has been proved to be a key link in the mechanism of morbidity. Intestinal dysbacteriosis directly contributes to lung injury through mechanisms such as microbial translocation, systemic inflammation, and immune dysregulation, and depletion of short-chain fatty acids (SCFAs) as key protective metabolites is an important driver of ARDS progression. SCFAs, mainly including acetate, propionate and butyrate, exert anti-inflammatory, immunomodulatory and barrier protective effects by inhibiting histone deacetylase (HDACs) and activating G protein-coupled receptors (GPCRs). However, SCFAs also exhibit concentration, type, and inflammation stage-dependent bidirectional regulatory properties. Clearly defining this bidirectional regulation is a critical factor for precision dosing and personalized therapies in a clinical setting. This article systematically reviews the causal mechanism of ARDS caused by intestinal flora imbalance, the bidirectional regulation of SCFAs, and the intervention strategies based on intestinal flora, providing new ideas for the precise treatment of sepsis-associated ARDS.Keywords: sepsis-associated ARDS, gut microbiota, SCFAs, gut-lung axis, immunomodulation
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