Project description:Viruses in acute exacerbations of idiopathic pulmonary fibrosis Keywords: viral detection BAL from patients with acute exacerbations of IPF and stable IPF were hybridized to a pan-viral cDNA microarray to evaluate the presence of virus during these episodes
Project description:Pulmonary fibrosis is a chronic progressive and often fatal disease. The pathogenesis is characterized by aberrant repair and remodeling of the lung parenchyma resulting in loss of physiological homeostasis, respiratory failure and death. The immune response in pulmonary fibrosis is dysregulated. The gut microbiome is a key regulator of immunity. The role of the gut microbiome in regulating the pulmonary immunity in lung fibrosis is unknown. Here, we have utilized a strategy of cage randomization to study how the horizontal transmission of gut microbiome influences the development of pulmonary fibrosis.
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.
Project description:Little is known about the lung microbiome dynamics and host-microbiome interactions in relation to chronic obstructive pulmonary disease (COPD) exacerbations and in patient subgroups based on smoking status and disease severity. Here we performed a 16S ribosomal RNA survey on sputum microbiome from 16 healthy and 43 COPD subjects. For COPD subjects, a longitudinal sampling was performed from stable state to exacerbations, at two and six weeks post-exacerbations and at six months from first stable visit. Host sputum transcriptome were characterized for a subset of COPD patient samples.
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
Project description:Pulmonary fibrosis is a progressive interstitial lung disease characterised by a progressive loss of lung function. It can occur as a result of occupational or medical exposures, genetic defects, trauma or acute lung injury leading to fibroproliferative acute respiratory distress syndrome, or it can occur in an idiopathic manner. The pathogenesis of each form of pulmonary fibrosis remains unclear. A variety of animal models have been developed to better understand the pathogenesis of pulmonary fibrosis. It has been shown that animal models of pulmonary fibrosis rely heavily on severe adverse effects induced by a variety of drugs, such as bleomycin, amiodarone, lipopolysaccharide and silica. The construction of animal models plays a key role in our understanding of the molecular mechanisms underlying the pathogenesis of PF, in outlining patient-specific pathology and in developing therapeutic strategies. However, the differences between models of pulmonary fibrosis induced by different drugs have rarely been investigated. Therefore, in this paper we performed single-cell sequencing analysis of animal models constructed from four drugs. The characteristics of the changes in the number of epithelial cells and macrophages and their functional enrichment in each model were summarised, and it was deduced that the model induced by lipopolysaccharide was mainly focused on the inflammatory damage stage of pulmonary fibrosis, the model induced by amiodarone on the regeneration stage of persistent failure, and the model induced by bleomycin and silica on the fibrotic stage of pulmonary fibrosis.