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: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:Impact of mass drug administration with azithromycin for trachoma elimination on prevalence and azithromycin resistance of genital Mycoplasma genitalium infection
Project description:Azithromycin has been shown to have anti-fibrotic effects on idiopathic lung fibroblasts (IPF). We thus wanted to investigate involved genes and pathways by microarray analysis. We treated normal human lung fibroblasts with Azithromycin (50uM) for 24h and compared them to non-treated samples.
Project description:Microarrays were used to evaluate the effects of azithromycin and an inflammatory stimulus (SMM) on human airway epithelium. Effects of azithromycin treatment were evaluated at 6, 24 and 48 hours. Effects of SMM were evaluated at 6 and 24 hours. In addition, pretreatment with azithromycin was used to evaluate the modulatory effects on SMM-induced inflammation. SMM=supernatant from microcorpulent material from human cystic fibrosis airways. Experiment Overall Design: 10 treatments total, 3-4 samples (patient codes = replicates) per treatment.
Project description:Microarrays were used to evaluate the effects of azithromycin and an inflammatory stimulus (SMM) on human airway epithelium. Effects of azithromycin treatment were evaluated at 6, 24 and 48 hours. Effects of SMM were evaluated at 6 and 24 hours. In addition, pretreatment with azithromycin was used to evaluate the modulatory effects on SMM-induced inflammation. SMM=supernatant from microcorpulent material from human cystic fibrosis airways. Keywords: timecourse, treatment comparisons.
Project description:Long-term, low dose azithromycin reduces exacerbation frequency in COPD yet the mechanism remains unclear. This study characterises changes to gene expression in patients with neutrophilic COPD in response to long term low dose azithromycin therapy. Patients with neutrophilic COPD (>61% or >162x10^4/mL sputum neutrophils) were randomised to 12 weeks of either azithromycin or placebo treatment. RNA was extracted from sputum and blood collected before (pre) and after (post) treatment.
Project description:Azithromycin binds to the nascent peptide exit tunnel (NPET) close to the peptidyltransferase center (PTC) of the ribosome, which obstructs the NPET and subsequently induces ribosome stalling and depletion of intracellular pools of tRNAs. To understand the mechanism through which azithromycin represses the transcription of mutation promoting genes, we utilized ribosome profiling to analyze azithromycin caused redistribution of ribosomes on the cellular mRNAs. Wild type PA14 was treated with 16 mg/L azithromycin for 3 hours.