https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36424 61% or >162x10⁴ cells per mL sputum neutrophils) were randomised to receive either azithromycin or placebo for 12 weeks. Sputum and blood were obtained before and after 12 weeks of treatment. Gene expression was defined using microarrays. Networks were analysed using the Search Tool for the Retrieval of Interacting Gene database. In sputum, 403 genes were differentially expressed following azithromycin treatment (171 downregulated and 232 upregulated), and three following placebo treatment (one downregulated and two upregulated) compared to baseline (adjusted p<0.05 by paired t-test, fold-change >1.5). In blood, 138 genes were differentially expressed with azithromycin (121 downregulated and 17 upregulated), and zero with placebo compared to baseline (adjusted p<0.05 by paired t-test, fold-change >1.3). Network analysis revealed one key network in both sputum (14 genes) and blood (46 genes), involving interferon-stimulated genes, human leukocyte antigens and genes regulating T-cell responses. Long-term, low-dose azithromycin is associated with downregulation of genes regulating antigen presentation, interferon and T-cell responses, and numerous inflammatory pathways in the airways and blood of neutrophilic COPD patients.]]> Thu 30 Apr 2020 12:50:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49090 Thu 04 May 2023 14:03:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47850 Thu 02 Feb 2023 16:46:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4857 Sat 24 Mar 2018 07:18:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22113 Sat 24 Mar 2018 07:13:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52693 256 mg/L) within 2 to 7 weeks and at 5 to 12 weeks, respectively. B. pertussis remained phenotypically susceptible to the antibiotic following 15 weeks of exposure, with the MIC between 0.032 to 0.38 mg/L. Genomic analysis revealed that B. holmesii developed resistance due to mutations in the 23S rRNA gene. The resistance mechanism in B. parapertussis was hypothesized as being due to upregulation of an efflux pump mechanism. Conclusions: These findings indicate that both B. holmesii and B. parapertussis can be more prone to induced resistance following exposure to treatment with erythromycin than B. pertussis. The surveillance of macrolide resistance in Bordetella isolates recovered from patients with pertussis, especially persistent disease, is warranted.]]> Fri 20 Oct 2023 15:55:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44511 Fri 14 Oct 2022 09:11:37 AEDT ]]>