Article Text
Abstract
The composition of the lung microbiome contributes to both health and disease, including obstructive lung disease. Because it has been estimated that over 70% of the bacterial species on body surfaces cannot be cultured by currently available techniques, traditional culture techniques are no longer the gold standard for microbial investigation. Advanced techniques that identify bacterial sequences, including the 16S ribosomal RNA gene, have provided new insights into the depth and breadth of microbiota present both in the diseased and normal lung. In asthma, the composition of the microbiome of the lung and gut during early childhood development may play a key role in the development of asthma, while specific airway microbiota are associated with chronic asthma in adults. Early bacterial stimulation appears to reduce asthma susceptibility by helping the immune system develop lifelong tolerance to innocuous antigens. By contrast, perturbations in the microbiome from antibiotic use may increase the risk for asthma development. In chronic obstructive pulmonary disease, bacterial colonisation has been associated with a chronic bronchitic phenotype, increased risk of exacerbations, and accelerated loss of lung function. In cystic fibrosis, studies utilising culture-independent methods have identified associations between decreased bacterial community diversity and reduced lung function; colonisation with Pseudomonas aeruginosa has been associated with the presence of certain CFTR mutations. Genomic analysis of the lung microbiome is a young field, but has the potential to define the relationship between lung microbiome composition and disease course. Whether we can manipulate bacterial communities to improve clinical outcomes remains to be seen.
- COPD mechanisms
- cystic fibrosis
- asthma
- bacterial infection
- COPD epidemiology
- COPD exacerbations
- emphysema
- interstitial fibrosis
- long term oxygen therapy (LTOT)
- lung transplantation
- lung volume reduction surgery
- pulmonary rehabilitation
- asthma guidelines
- asthma mechanisms
- perception of asthma/breathlessness
- respiratory infection
- viral infection
- allergic lung disease
- COPD pathology
- cytokine biology
- innate immunity
- lymphocyte biology
- macrophage biology
- tobacco and the lung
- viral infection
- COPD pharmacology
- pneumonia
- pneumonia
- asthma epidemiology
- asthma genetics
- lung physiology
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- COPD mechanisms
- cystic fibrosis
- asthma
- bacterial infection
- COPD epidemiology
- COPD exacerbations
- emphysema
- interstitial fibrosis
- long term oxygen therapy (LTOT)
- lung transplantation
- lung volume reduction surgery
- pulmonary rehabilitation
- asthma guidelines
- asthma mechanisms
- perception of asthma/breathlessness
- respiratory infection
- viral infection
- allergic lung disease
- COPD pathology
- cytokine biology
- innate immunity
- lymphocyte biology
- macrophage biology
- tobacco and the lung
- viral infection
- COPD pharmacology
- pneumonia
- pneumonia
- asthma epidemiology
- asthma genetics
- lung physiology
Footnotes
Dr Toews died on 12th Oct 2011.
Funding MKH is supported by NHLBI grant K23 HL093351. YJH is supported by NIH/NHLBI grant 1K23HL105572-01 and a Cystic Fibrosis Foundation PACE award. JJL is supported by NIH/NHLBI grant 1RC1HL100809-01 and CTSA grant UL1RR024986 and the Cystic Fibrosis Foundation. JLC is supported by NIH/NHLBI grant R01 HL082480 and by a Research Enhancement Award Program from the Biomedical Laboratory Research & Development Service, Department of Veterans Affairs. GBH is supported by grants RO1-AI064479, R21-AI087869, R21-AI083473, R21-AI087869 and P30-DK034933. FJM is supported by NIH/NHLBI contracts HHSN2682011008C and HHSN268200900016C. SVL is supported by grants AI075410, U01HL098964, AI113916, R21AT004732, PBBR, CFF and CFRI awards. VBY is supported by grants UH3 DK083993, U19 AI090871, U01 HL098961, R01 DK070875 and P30 DK034933.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.