Imbalance of Intestinal Flora Activates Inflammatory Response Contributing to Acute Lung Injury
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE255726 | GEO | 2024/07/31
REPOSITORIES: GEO
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Project description:BackgroundSeawater 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.MethodsSeawater 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.ResultsThe 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 Firmicutes and decreasing that of Bacteroidota. Transcriptional upregulation of inflammatory responses in ALI mice was observed in the lung transcriptome, and differentially expressed genes were mainly enriched in inflammation-related pathways such as cytokine-cytokine receptor interaction, viral protein interaction with cytokine and cytokine receptor, and chemokine signaling pathway, which were further confirmed by microbe-gene association analysis. Furthermore, inflammatory factors were up-regulated, oxidative stress molecule MDA was elevated, and SOD was decreased in the lung tissues of mice, suggesting that the imbalance of intestinal flora activated inflammatory and oxidative stress responses.ConclusionsThis 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.
| S-EPMC11565338 | biostudies-literature
Project description:Imbalance of Intestinal Flora Activates Inflammatory Response Contributing to Acute Lung Injury
| PRJNA1076234 | ENA
Project description:BackgroundThe gut microbiota participates in the metabolism of substances and energy, promotes the development and maturation of the immune system, forms the mucosal barrier, and protects the host from pathogen attacks. Although the pathogenesis of cholesterol gallstones is still not clear, studies have suggested that gut microbiota dysbiosis plays an important role in their formation.MethodsMicrobial DNA from faeces of normal control patients and those of patients with calculi was subjected to 16S rRNA gene sequencing to detect gene expression changes in intestinal microbes. ELISA kits were used to measure free bile acids, secondary bile acids and coprostanol according to the manufacturer's instructions. The relationship between flora and their metabolites was then analysed.ResultsIn the gallstone group, the diversity of intestinal bacteria and the abundances of certain phylogroups were significantly decreased (p < 0.05), especially Firmicutes (p < 0.05), the largest phylum represented by the gut microbiota. This study found an increase in free bile acids (p < 0.001) and secondary bile acids (p < 0.01) in the enterohepatic circulation. Bile salt hydrolase activity was not related to the abundances of BSH-active bacteria. 7a-dehydroxylating gut bacteria were significantly increased (p < 0.01), whereas cholesterol-lowering bacteria were significantly reduced (p < 0.05). The Ruminococcus gnavus group could be used as a biomarker to distinguish the gallstone group from the control group.ConclusionWe conclude that intestinal flora imbalance affects bile acid and cholesterol metabolism and is associated with gallstone formation.
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Project description:Nigella A, also named Sieboldianoside A, has been extracted from many kinds of Traditional Chinese Medicine (TCM), such as Nigella glandulifera, Stauntonia chinensis DC., and the leaves of Acanthopanax sieboldianus. Nigella A exhibited potential analgesic, anti-inflammatory, anti-tumor, and antioxidant activities. However, whether Nigella A could treat ulcerative colitis (UC) is still unknown. As saponins always be regarded as the kinds of ingredients that could regulate immunity and intestinal flora. This research aimed to investigate the therapeutic effect of Nigella A on UC and explore its effect on intestinal flora. We noted that Nigella A and Sulfasalazine (SASP) could significantly improve the signs and symptoms, alleviate colonic pathological injury in DSS-induced mice. The changing of many specific bacterial genus such as Lactobacillus, Porphyromonadaceae, Bacteroides and Escherichia might closely related to the recovery of intestinal inflammatory response. This study initially confirmed the therapeutic effect of Nigella A and SASP on DSS-induced colitis by improving the diversity of intestinal microbial composition. Nigella A has the potential to be developed for the treatment of UC and other disorders related to the imbalance of intestinal flora.
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Project description:Groupers with an initial body weight of 9.10 ± 0.03 g were selected to investigate whether dietary addition of 0 (G0) and 1800 mg/kg glycerol monolaurate (GML, G1800) could alleviate the oxidative stress response and intestinal flora imbalance after 0, 6, 12, and 24 h of salinity change in grouper. Experimental results show that the dietary addition of GML significantly reduced the liver MDA content and increased the SOD activity of grouper. The gene expression of CAT and SOD increased and then decreased with time after adding 1800 mg/kg GML, and the highest values were significantly higher than those of the control group. Salinity change had a slight effect on the top four intestinal flora composition of grouper at 0, 12, and 24 h, with changes occurring only at 6 h when Cyanobacteria replaced Actinobacteria. The addition of dietary GML slowed down the intestinal flora disorder, inhibited the colonization of harmful bacterium Vibrio, and promoted the abundance of beneficial bacterium Bacillus. In conclusion, dietary GML significantly reduced the oxidative damage caused by sudden changes in salinity, improved the antioxidant capacity, and alleviated the intestinal flora imbalance in juvenile grouper.
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Project description:Hepatic ischemia-reperfusion IR (HIR) is an unavoidable pathophysiological process during liver transplantation, resulting in systematic sterile inflammation and remote organ injury. Acute lung injury (ALI) is a serious complication after liver transplantation with high postoperative morbidity and mortality. However, the underlying mechanism is still unclear. To assess the phenotype and plasticity of various cell types in the lung tissue microenvironment after HIR at the single-cell level, single-cell RNA sequencing (scRNA-seq) was performed using the lungs from HIR-induced mice.
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