ArticleFrontiers in microbiology2025
Gut microbiota dysbiosis aggravates sepsis-induced lung injury by promoting neutrophil extracellular traps and suppressing host integrin defense.
Article in Frontiers in microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Article
- Circadian clock-gut microbiota axis in pulmonary hypertension: linking gut-lung crosstalk, immune timing and vascular remodeling.Frontiers in physiology · 2026Review
- Source-stratified gut-extraintestinal organ crosstalk in sepsis-associated acute gastrointestinal injury and paralytic ileus: the gut as both driver and target.Frontiers in medicine · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
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Abstract
Background: The gut-lung axis is central to systemic inflammatory regulation, but the mechanisms by which gut microbiota dysbiosis aggravates sepsis-induced acute lung injury (ALI), particularly through neutrophil extracellular traps (NETs) and integrin signaling, remain unclear. Given the critical need for microbiota-based therapeutic strategies, this study investigates the mechanistic link between gut microbiota, NET formation, and pulmonary endothelial barrier dysfunction. Methods: Using a cecal ligation and puncture (CLP) sepsis model, control, sepsis, and fecal microbiota transplantation (FMT) groups were compared. Lung injury was assessed via histopathology, wet/dry weight ratios, and bronchoalveolar lavage fluid (BALF) analysis. High-throughput RNA sequencing (GO/KEGG/PPI) identified key targets, validated by lentiviral knockdown/overexpression of ITGAM and ITGB2 Results: CLP-induced sepsis triggered severe pulmonary edema, neutrophil infiltration, and NET accumulation, alongside downregulation of ITGAM/ITGB2 and tight junction proteins (β-catenin/ZO-1/VE-cadherin). FMT reduced NETs by 58% ( Conclusion: We unveil a novel gut microbiota-NET-integrin axis in sepsis-induced ALI, where microbial dysbiosis promotes NET-mediated suppression of ITGAM/ITGB2, leading to endothelial barrier failure. Our findings position FMT and integrin modulation as promising strategies to mitigate pulmonary vascular dysfunction, advancing the therapeutic potential of microbiota-targeted interventions in critical care.
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