ArticleAmerican journal of respiratory cell and molecular biology2026
Reduction of palmitoleic acid due to changes in pulmonary microbiota contributes to acute lung injury after single-lung ventilation.
Article in American journal of respiratory cell and molecular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Palmitoleic acid loss links pulmonary dysbiosis to lung injury after single-lung ventilation.American journal of respiratory cell and molecular biology · 2026Article
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9 authors.
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Abstract
backgroundSingle-lung ventilation (SLV), commonly used in thoracic surgery, carries a risk of acute lung injury and acute respiratory distress syndrome. Our previous studies suggest that pulmonary microbiota may play a role in SLV-induced lung injury, but the precise mechanisms remain unclear. Palmitoleic acid (PoA), a crucial metabolite, is associated with protective physiological processes. This study explores the variations in pulmonary microbiota and metabolites during SLV-induced lung injury and investigates the potential protective role of PoA.
resultsThe development of SLV-induced lung injury correlated with the changes of pulmonary microbiota and alterations of certain microbial genera and species. Through metabolomics and correlation analysis of pulmonary metabolites and microbiota, several metabolites exhibited a negative association with SLV-induced lung injury, with PoA being particularly noteworthy. Changes in pulmonary microbiota appeared to contribute to the reduction of PoA levels, ultimately leading to lung injury. Supplementation with PoA significantly attenuated the severity of lung injury, both in vivo and in vitro, by upregulating PPARγ expression and its downstream signaling pathways.
conclusionsThe dysregulation of pulmonary microbiota contributes to SLV-induced lung injury, with PoA reduction playing a role in this process. PoA supplementation offers a protective effect by activating the PPAR pathway, suggesting its therapeutic potential in mitigating SLV-induced lung injury.
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