The Lung Tissue Microbiome in Chronic Obstructive Pulmonary Disease

Sze, Marc A.; Dimitriu, Pedro A.; Hayashi, Shizu; Elliott, W. Mark; McDonough, John E.; Gosselink, John V.; Cooper, Joel D.; Sin, Don D.; Mohn, William W.; Hogg, James C.

doi:10.1164/rccm.201111-2075oc

Cited by 469 publications

(480 citation statements)

References 52 publications

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“…It seems likely that a minority of COPD patients and controls exhibit low microbial diversity, and these samples may skew the results of studies with small sample sizes. Our results are consistent with Sze et al, who showed that patients with Very Severe COPD maintained greater microbial diversity than control subjects [16]. Our data show that age, rather than severity of COPD, is associated with increased microbial diversity.…”

Section: Discussionsupporting

confidence: 93%

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The Lung Microbiome in Moderate and Severe Chronic Obstructive Pulmonary Disease

Pragman¹,

Kim²,

Reilly³

et al. 2014

Annals ATS

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Chronic obstructive pulmonary disease (COPD) is an inflammatory disorder characterized by incompletely reversible airflow obstruction. Bacterial infection of the lower respiratory tract contributes to approximately 50% of COPD exacerbations. Even during periods of stable lung function, the lung harbors a community of bacteria, termed the microbiome. The role of the lung microbiome in the pathogenesis of COPD remains unknown. The COPD lung microbiome, like the healthy lung microbiome, appears to reflect microaspiration of oral microflora. Here we describe the COPD lung microbiome of 22 patients with Moderate or Severe COPD compared to 10 healthy control patients. The composition of the lung microbiomes was determined using 454 pyrosequencing of 16S rDNA found in bronchoalveolar lavage fluid. Sequences were analyzed using mothur, Ribosomal Database Project, Fast UniFrac, and Metastats. Our results showed a significant increase in microbial diversity with the development of COPD. The main phyla in all samples were Actinobacteria, Firmicutes, and Proteobacteria. Principal coordinate analyses demonstrated separation of control and COPD samples, but samples did not cluster based on disease severity. However, samples did cluster based on the use of inhaled corticosteroids and inhaled bronchodilators. Metastats analyses demonstrated an increased abundance of several oral bacteria in COPD samples.

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Section: Discussionsupporting

confidence: 93%

“…They noted increased bacterial diversity in the COPD patients compared to controls. COPD patients had an increase in the phylum Firmicutes, attributable to an increase in Lactobacillus [16].…”

Section: Introductionmentioning

confidence: 99%

The Lung Microbiome in Moderate and Severe Chronic Obstructive Pulmonary Disease

Pragman¹,

Kim²,

Reilly³

et al. 2014

Annals ATS

View full text Add to dashboard Cite

show abstract

“…COPD pathogenetic mechanisms are constantly revisited and now include some novel aspects, e.g. shifts in lung microflora (Sze et al 2012), autoimmune component of the disease (Cosio et al 2002) and other than cigarette smoke environmental risk factors, that include indoor and outdoor air pollution, dust and fumes (Forbes et al 2009;Hopkinson and Polkey 2015). Scientific community still lacks a holistic understanding of COPD development and only several mechanisms are well described and generally recognized, i.e.…”

Section: Introductionmentioning

confidence: 99%

Native matrix-based human lung alveolar tissue model in vitro: studies of the reparatory actions of mesenchymal stem cells

et al. 2016

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Studies of lung diseases in vitro often rely on flat, plastic-based monocultures, due to short lifespan of primary cells, complicated anatomy, lack of explants, etc. We hereby present a native 3D model with cues for repopulating epithelial cells. Abilities of mesenchymal stem cells (MSC) to modulate bacterial lipopolysaccharide (LPS) and cigarette smoke-induced injury to pulmonary epithelium were tested in our model. Post-mortem human lung tissue was sliced, cut and decellularized. Resulting matrix pads were reseeded with pulmonary epithelium (A549 line). Markers of the layer integrity and certain secreted proteins in the presence of cigarette smoke extract (CSE) and LPS were assessed via Western blot, ELISA and RT-PCR assays. In parallel, the effects of MSC paracrine factors on exposed epithelial cells were also investigated at gene and protein levels. When cultured on native 3D matrix, A549 cells obtain dual, type I-and II-like morphology. Exposure to CSE and LPS leads to downregulation of several epithelial proteins and suppressed proliferation rate. MSC medium added to the model restores proliferation rate and some of the epithelial proteins, i.e. e-cadherin and beta-catenin. CSE also increases secretion of proinflammatory cytokines by epithelial cells and upregulates transcription factor NFjB. Some of these effects might be counteracted by MSC in our model. We introduce repopulated decellularized lung matrix that highly resembles in vivo situation and is convenient for studies of disease pathogenesis, cytotoxicology and for exploring therapeutic strategies in the human lung context in vitro. MSC paracrine products have produced protecting effects in our model.

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“…La colonisation bactérienne est un facteur important contribuant à la progression de la BPCO [29] et à la survenue des exacerbations infectieuses [7]. De nombreuses pistes ont été décrites pour expliquer comment l'exposition tabagique détruit les défenses pulmonaires de l'hôte via la suppression de la production de peptides antimicrobiens, la destruction de la barrière épithéliale et la colonisation des voies aériennes inférieures par un certain nombre d'agents microbiologiques [25,30,31] [33]. Le microbiote est également modifié par l'antibiothérapie et la corticothérapie [24].…”

Section: Microbiome Pulmonaire Et Broncho-pneumopathie Chronique Obstunclassified

“…À l'inverse, la colonisation par des bactéries sélectionnées serait un facteur de risque accru pour l'asthme. L'impact de la colonisation bactérienne sur l'asthme et sur la survenue d'exacerbations, a été observé dans de nombreuses études avec des taux de colonisation allant de 12 à 61 % selon les résultats [43][44][45] soit (mucoviscidose, BPCO, ou asthme), la survenue d'une exacerbation sera associée à une modification du bactériote et du bactériome, voire du mycobiote et/ou du virome [8,9,11,14,31,33,34]. Cette dysbiose, largement étudiée en ce qui concerne la communauté bactérienne, moins documentée pour les micromycètes, les virus ou les phages, montre clairement son impact sur la fonction respiratoire, sur la réponse inflammatoire et immune locale, voire une association avec une réponse incomplète au traitement adapté à la pathologie pulmonaire [23].…”

Section: Microbiome Pulmonaire Et Asthmeunclassified

Le microbiome pulmonaire en 2015

Andréjak

Delhaès

2015

Med Sci (Paris)

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The Lung Tissue Microbiome in Chronic Obstructive Pulmonary Disease

Cited by 469 publications

References 52 publications

The Lung Microbiome in Moderate and Severe Chronic Obstructive Pulmonary Disease

The Lung Microbiome in Moderate and Severe Chronic Obstructive Pulmonary Disease

Native matrix-based human lung alveolar tissue model in vitro: studies of the reparatory actions of mesenchymal stem cells

Le microbiome pulmonaire en 2015

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