Homo sapiens
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PROVIDER: PRJNA210948 | ENA |
REPOSITORIES: ENA
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Project description:Enrichment of lung microbiome with supraglottic taxa is associated with increased pulmonary inflammation
| PRJNA210947 | ENA
Project description:<p><b>Background</b>: The lung microbiome of healthy individuals frequently harbors oral organisms. Despite evidence that micro-aspiration is commonly associated with smoking-related lung diseases, the effects of lung microbiome enrichment with upper airway taxa on inflammation has not been studied. We hypothesize that the presence of oral microorganisms in the lung microbiome is associated with enhanced pulmonary inflammation.</p> <p><b>Methods</b>: We sampled bronchoalveolar lavage (BAL) from the lower airways of 29 asymptomatic subjects (9 never-smokers, 14 former-smokers and 6 current-smokers). We quantified, amplified, and sequenced 16S rRNA genes from BAL samples by qPCR and 454 sequencing. Pulmonary inflammation was assessed by exhaled nitric oxide (eNO), BAL lymphocytes and neutrophils.</p> <p><b>Results</b>: BAL had lower total 16S than supraglottic samples and higher than saline background. Bacterial communities in the lower airway clustered in two distinct groups that we designated as pneumotypes. The rRNA gene concentration and microbial community of the first pneumotype was similar to that of the saline background. The second pneumotype had higher rRNA gene concentration and higher relative abundance of supraglottic-characteristic taxa (SCT), such as Veillonella and Prevotella, and we called it pneumotypeSCT. Smoking had no effect on pneumotype allocation, alpha or beta diversity. PneumotypeSCT was associated with higher BAL lymphocyte-count (p = 0.007), BAL neutrophil-count (p = 0.034) and eNO (p = 0.022).</p> <p><b>Conclusion</b>: A pneumotype with high relative abundance of supraglottic-characteristic taxa is associated with enhanced subclinical lung inflammation. </p>
| phs000633 | dbGaP
Project description:Azithromycin (AZM) reduces pulmonary inflammation and exacerbations in chronic obstructive pulmonary disease patients with emphysema. The antimicrobial effects of AZM on the lung microbiome are not known and may contribute to its beneficial effects. Methods. Twenty smokers with emphysema were randomized to receive AZM 250 mg or placebo daily for 8 weeks. Bronchoalveolar lavage (BAL) was performed at baseline and after treatment. Measurements included: rDNA gene quantity and sequence. Results. Compared with placebo, AZM did not alter bacterial burden but reduced α-diversity, decreasing 11 low abundance taxa, none of which are classical pulmonary pathogens. Conclusions. AZM treatment the lung microbiome Randomized trial comparing azithromycin (AZM) treatment with placebo for eight weeks. Bronchoalveolar lavage (BAL) samples were obtained before and after treatment to explore the effects of AZM on microbiome, in the lower airways. 16S rRNA was quantified and sequenced (MiSeq) The amplicons from total 39 samples are barcoded and the barcode is provided in the metadata_complete.txt file.
2016-07-19 | E-GEOD-74396 | biostudies-arrayexpress
Project description:Azithromycin (AZM) reduces pulmonary inflammation and exacerbations in chronic obstructive pulmonary disease patients with emphysema. The antimicrobial effects of AZM on the lung microbiome are not known and may contribute to its beneficial effects. Methods. Twenty smokers with emphysema were randomized to receive AZM 250 mg or placebo daily for 8 weeks. Bronchoalveolar lavage (BAL) was performed at baseline and after treatment. Measurements included: rDNA gene quantity and sequence. Results. Compared with placebo, AZM did not alter bacterial burden but reduced α-diversity, decreasing 11 low abundance taxa, none of which are classical pulmonary pathogens. Conclusions. AZM treatment the lung microbiome
2016-07-19 | GSE74396 | GEO
Project description:Idiopathic pulmonary fibrosis (IPF) is a devastating pulmonary disease with no curative treatment other than lung transplantation. IPF results from maladaptive responses to lung epithelial injury, but the underlying mechanisms remain unclear. Here, we show that deficiency in the innate immune receptor, toll-like receptor 5 (TLR5), is associated with IPF in humans and with increased susceptibility to experimental fibrosis in mice, while activation of lung epithelial TLR5 through a synthetic flagellin analog protects from experimental fibrosis. Mechanistically, epithelial TLR5 activation induces antimicrobial gene expression and ameliorates dysbiosis after lung injury. In contrast, TLR5 deficiency in mice and IPF patients is associated with lung dysbiosis. Elimination of the microbiome in mice through antibiotics abolishes the protective effect of TLR5 and reconstitution of the microbiome rescues the observed phenotype. In aggregate, TLR5 deficiency is associated with IPF and dysbiosis in humans and in the murine model of pulmonary fibrosis. Furthermore, TLR5 protects against pulmonary fibrosis in mice, and this protection is mediated by effects on the microbiome.
2026-04-03 | GSE314583 | GEO
Project description:Asthma is a chronic inflammatory airway disease characterized by airway inflammation and remodeling. The role of 15-oxo-5Z,8Z,11Z,13E-eicosatetraenoic acid (15-oxoETE), a 15-HETE metabolite catalyzed by 15-prostaglandin dehydrogenase (15-PGDH), has been relatively unexplored in asthma. In this study, we used RNA-seq to explore the effect of 15-KETE on the transcriptome of airway epithelial cells, aiming to identify its potential downstream targets and mechanisms of action.
2026-05-21 | GSE325003 | GEO
Project description:Background: Artemisia argyi is a traditional medicinal herb with established anti-inflammatory and immunomodulatory properties. Its aqueous extract (AEAA), enriched in water-soluble bioactive constituents, exhibits favorable safety and bioavailability; however, its potential protective effects against acute lung injury (ALI) and its associations with systemic immunometabolic regulation remain incompletely understood. Methods: An LPS-induced ALI mouse model was established following 28 days of AEAA pretreatment. Lung histopathology, pulmonary edema, and inflammatory cytokines were evaluated. Integrated multi-omics analyses—including gut microbiota profiling, untargeted metabolomics of colonic contents and serum, and lung transcriptomics—were performed to characterize treatment-associated microbial, metabolic, and transcriptional alterations. Results: AEAA pretreatment dose-dependently alleviated lung injury, reduced pulmonary edema, and suppressed pro-inflammatory cytokines while restoring anti-inflammatory IL-10 levels. AEAA treatment was associated with partial reversal of LPS-induced gut dysbiosis, characterized by reduced abundance of inflammation-associated taxa and enrichment of beneficial genera, particularly Akkermansia and Lactobacillus. Metabolomic analyses revealed treatment-associated normalization of intestinal and systemic metabolic disturbances, including increased homeostasis-related metabolites and reduced inflammation-associated metabolites. Lung transcriptomic profiling suggested attenuation of LPS-associated transcriptional signatures related to NF-κB, MAPK, Toll-like receptor, and PI3K–AKT signaling pathways. Cross-omics integration further revealed coordinated associations among microbial shifts, metabolic remodeling, and pulmonary inflammatory gene expression. Conclusion: These findings suggest that aqueous Artemisia argyi extract is associated with mitigation of LPS-induced acute lung injury, accompanied by coordinated alterations in gut microbiota composition, host metabolic profiles, and pulmonary inflammatory gene expression. Although causal relationships were not established, this integrated multi-omics analysis provides a systems-level, hypothesis-generating framework supporting the potential of AEAA as a multi-target botanical candidate for ALI.
2026-03-27 | MTBLS14160 | MetaboLights
Project description:In this study, we assessed lower airway microbiome from a cohort of patients to determine whether specific microbiome taxa correlate with with specific metabolic activities. In a subset of 12 patients, transcriptomic expression were analyzed to compare host mucosa immune response We collected peripheral airway brushings from the 12 subjects whose lung microbiome were analyzed; Total RNA were obtained from the peripheral airway epithelium.
2016-03-29 | E-GEOD-73585 | biostudies-arrayexpress
Project description:Chronic obstructive pulmonary disease (COPD) is associated with airway inflammation and microbiota dysbiosis. However, the function of lung microbiome alteration in early COPD remains unclear. This study is the first to characterize the lower respiratory tract microbiota in early COPD patients via bronchoalveolar lavage fluid (BALF) samples. By using full-length 16S sequencing, we found that the lung microbiome of early COPD patients had lower bacterial richness and significant compositional differences than did that of the healthy smoker controls. Streptococcus was the most robustly distinguished genus in early COPD patients and was associated with decreased lung function and increased host local inflammation. Furthermore, a murine cigarette smoke model of early COPD revealed that Streptococcus mitis promotes the progression of early COPD. Single-cell transcriptomics revealed that Streptococcus mitis increased emphysematous destruction of the lung parenchyma in a mouse early COPD model by regulating the function of alveolar type II (AT2) cells and macrophages. Therefore, targeting the lower airway microbiota in combination with smoking cessation may be a potential therapeutic approach for early COPD.
2025-03-02 | GSE290402 | GEO
Project description:The Forkhead Box f1 (Foxf1) transcriptional factor (previously known as HFH-8 or Freac-1) is expressed in endothelial and smooth muscle cells in the embryonic and adult lung. To assess effects of Foxf1 during lung injury, we used CCl4 injury model. Foxf1+/- mice developed severe airway obstruction and bronchial edema, associated with increased numbers of pulmonary mast cells and increased mast cell degranulation following injury. Pulmonary inflammation in Foxf1+/- mice was associated with diminished expression of Foxf1, increased mast cell tryptase and increased expression of CXCL12, the latter being essential for mast cell migration and chemotaxis. Foxf1 haploinsufficiency caused pulmonary mastocytosis and enhanced pulmonary inflammation following chemically-induced lung injury, indicating an important role for Foxf1 in the pathogenesis of pulmonary inflammatory responses. Keywords: Influence of genetic modification on the pulmonary inflamation Foxf1+/- mice in which the Foxf1 allele was disrupted by an in-frame insertion of a nuclear localizing -galactosidase (-Gal) gene were bred for ten generations into the Black Swiss mouse genetic background. Carbon tetrachloride (CCl4; Sigma, St Louis, MO) was dissolved in mineral oil at a 1:20 ratio v/v and a single intraperitoneal (i.p.) injection of CCl4 (0.5 l of CCl4/ 1g of body weight) was administered to male Foxf1+/- mice or their wild type (WT) littermates as described.
2008-09-04 | E-GEOD-11112 | biostudies-arrayexpress