ArticleACS omega2025
Xuanfei Baidu Decoction Alleviated Sepsis-Induced ALI by Modulating Gut Microbial Homeostasis and Promoting Inflammation Resolution: Bioinformatics and Experimental Study.
Article in ACS omega, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Single-Cell and Spatial Transcriptomics Identify the Mono-S100A4 Subset Associated with Sepsis-Induced Lung Injury via the MIF-(CD74+CD44) Axis.Journal of inflammation research · 2026Article
- Gut microbiota in acute lung injury/acute respiratory distress syndrome: mechanistic insights and therapeutic opportunities via the gut-lung axis.Frontiers in cellular and infection microbiology · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Xuanfei Baidu Decoction (XFBD) has shown effective therapeutic potential for acute lung injury (ALI) induced by lipopolysaccharide and immunoglobin G immune complexes. Herein, the protective effects and mechanisms of XFBD were investigated in a sepsis-induced ALI mouse model along with its effects on gut microbiota. Notably, bioinformatics and molecular docking analyses revealed that XFBD components exhibited a strong binding affinity to G-protein-coupled receptor 18 (GPR18). In the murine ALI model-induced by cecal ligation and puncture (CLP)-XFBD markedly improved lung histopathology, reduced M1 macrophage polarization, and decreased pro-inflammatory cytokine levels in both lung tissues and MH-S macrophages. Furthermore, XFBD downregulated key inflammatory pathways, including nuclear factor (NF)-κB, phosphorylated-NF-κB, CCAAT/enhancer binding protein-δ, and the nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3/Caspase-1/gasdermin D axis. Additionally, XFBD restored the CLP-induced disruption in gut microbiota balance, increasing the abundance of Prevotellaceae and Ruminococcaceae_UCG_014. Altogether, the findings of this study suggest that XFBD alleviates CLP-induced ALI by modulating gut microbial homeostasis and inhibiting associated inflammatory pathways, particularly via GPR18 activation, presenting the promising therapeutic potential of XFBD for treating sepsis-induced ALI.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.