ArticleInternational journal of chronic obstructive pulmonary disease2020
COPD-Related Modification to the Airway Epithelium Permits Intracellular Residence of Nontypeable
Article in International journal of chronic obstructive pulmonary disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Human airway organoids for bacterial-host interaction studies: methods, insights and translational promise.Thorax · 2026Review
- Autophagy Is Suppressed in Peripheral Blood Mononuclear Cells During Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2026Article
- Exploring microorganism-host interactions: Emerging organoid models and analytical approaches.mLife · 2026Review
- Wenshen Yiqi Granule Alleviates Chronic Obstructive Pulmonary Disease via the Long Noncoding RNA-XIST/MicroRNA-200c-3p Axis.Pulmonary circulation · 2025Article
- In vitro modelling of bacterial pneumonia: a comparative analysis of widely applied complex cell culture models.FEMS microbiology reviews · 2024Review
- Time to re-set our thinking about airways disease: lessons from history, the resurgence of chronic bronchitis / PBB and modern concepts in microbiology.Frontiers in pediatrics · 2024Review
- Article
- Organotypic sinonasal airway culture systems are predictive of the mucociliary phenotype produced by bronchial airway epithelial cells.Scientific reports · 2022Article
- Journal Club: Biologics and Potential for Immune Modulation in Chronic Obstructive Lung Disease.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2022Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: COPD is an inflammatory airway pathology associated with recurrent infection by nontypeable Methods: Cultures of bronchial airway epithelial cells derived from control and COPD participants were differentiated at an air-liquid interface and exposed to macrolide antibiotics, 10% cigarette smoke-extract (CSE) and NTHi. Markers of autophagic flux and intracellular NTHi were assessed using Western blot analysis and transmission electron microscopy. Results: AEC treated with macrolide antibiotics or 10% CSE exhibited a block in autophagic flux as evidenced by a concomitant increase in LC3-II and Sequestosome abundance (vs control; both P < 0.01). While control AEC showed no clear evidence of intracellular NTHi, COPD-derived cultures exhibited abundant NTHi within the cytoplasm. Further, intracellular NTHi that were encapsulated within vesicles propagated from the apical epithelial layer to the basal cell layer. Discussion: Taken together, our findings indicate that COPD, cigarette smoke and macrolide antibiotics potentiate the susceptibility to persistent intracellular NTHi. A major mechanism for this is arresting normal autophagic flux in airway epithelial cells. Hence, structural modifications that mitigate this off-target effect of macrolides have significant potential to clear intracellular NTHi and thereby reduce the influence of this pathogen in the airways afflicted by COPD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.