ArticleJournal of thoracic disease2024
Imbalance of intestinal flora activates inflammatory response contributing to acute lung injury.
Article in Journal of thoracic disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Article
- Chaiyin Granules Improve Acute Lung Injury by Regulating Gut Microbiota and Unsaturated Fatty Acid Mediated Wnt/β-Catenin Signaling Pathway.Journal of immunology research · 2026Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Seawater drowning is a leading cause of accidental injury and death, and the resulting acute lung injury (ALI) is a serious clinical syndrome for which there are no effective treatments. This study aims to investigate the potential mechanism of seawater drowning-induced ALI. Methods: Seawater drowning mouse models were constructed to assess lung injury. The hematoxylin & eosin (H&E) staining and fluorescent terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were used to observe the pathology of lung tissues and apoptosis, respectively. 16S rRNA and RNA-seq were performed to identify the structure of the intestinal microbes and the gene expression profiles of the lung tissue of the mice, respectively. The expression of cytokines was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA), and the activities of superoxide dismutase (SOD) and malondialdehyde (MDA) were detected by assay kits. Results: The results showed that seawater drowning aggravated lung injury and accelerated cell apoptosis in mice. Seawater exposure significantly altered the structure of mouse intestinal microbes, especially increasing the abundance of Conclusions: This study reveals the mechanism that intestinal microflora aggravates ALI by modulating inflammatory signaling pathways, depicting the landscape of the microbial-gene-lung axis and providing new insights into the use of gut flora as a therapeutic strategy for ALI.
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