期刊
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
卷 188, 期 10, 页码 1224-1231出版社
AMER THORACIC SOC
DOI: 10.1164/rccm.201302-0341OC
关键词
rhinovirus; chronic obstructive pulmonary disease; bacteria; microbiome
资金
- Asmarley Charitable Trust
- Medical Research Council [G0600879]
- Wellcome Trust [083567/Z/07/Z, 096964/Z/11/Z]
- Imperial College and the National Institute for Health Research (NIHR) Biomedical Research Centre
- NIHR
- GlaxoSmithKline
- Pfizer UK
- Wellcome Trust [096964/Z/11/Z, 083567/Z/07/Z] Funding Source: Wellcome Trust
- MRC [G0600879] Funding Source: UKRI
- Medical Research Council [G1000758, G0600879] Funding Source: researchfish
- National Institute for Health Research [CL-2008-21-014, NF-SI-0512-10126] Funding Source: researchfish
Rationale: Rhinovirus infection is followed by significantly increased frequencies of positive, potentially pathogenic sputum cultures in chronic obstructive pulmonary disease (COPD). However, it remains unclear whether these represent de novo infections or an increased load of organisms from the complex microbial communities (microbiome) in the lower airways. Objectives: To investigate the effect of rhinovirus infection on the airway bacterial microbiome. Methods: Subjects with COPD (n = 14) and healthy control subjects with normal lung function (n = 17) were infected with rhinovirus. Induced sputum was collected at baseline before rhinovirus inoculation and again on Days 5, 15, and 42 after rhinovirus infection and DNA was extracted. The V3-V5 region of the bacterial 16S ribosomal RNA gene was amplified and pyrosequenced, resulting in 370,849 high-quality reads from 112 of the possible 124 time points. Measurements and Main Results: At 15 days after rhinovirus infection, there was a sixfold increase in 16S copy number (P = 0.007) and a 16% rise in numbers of proteobacterial sequences, most notably in potentially pathogenic Haemophilus influenzae (P = 2.7 x 10(-20)), from a preexisting community. These changes occurred only in the [GRAPHICS] sputum microbiome of subjects with COPD and were still evident 42 days after infection. This was in contrast to the temporal stability demonstrated in the microbiome of healthy smokers and nonsmokers. Conclusions: After rhinovirus infection, there is a rise in bacterial burden and a significant outgrowth of Haemophilus influenzae from the existing microbiota of subjects with COPD. This is not observed in healthy individuals. Our findings suggest that rhinovirus infection in COPD alters the respiratory microbiome and may precipitate secondary bacterial infections.
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