The lung tissue microbiota of mild and moderate chronic obstructive pulmonary disease
Abstract Background Oral taxa are often found in the chronic obstructive pulmonary disease (COPD) lung microbiota, but it is not clear if this is due to a physiologic process such as aspiration or experimental contamination at the time of specimen collection. Methods Microbiota samples were obtained...
| Main Authors: | , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
BMC
2018-01-01
|
| Series: | Microbiome |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s40168-017-0381-4 |
| _version_ | 1818418895490383872 |
|---|---|
| author | Alexa A. Pragman Tianmeng Lyu Joshua A. Baller Trevor J. Gould Rosemary F. Kelly Cavan S. Reilly Richard E. Isaacson Chris H. Wendt |
| author_facet | Alexa A. Pragman Tianmeng Lyu Joshua A. Baller Trevor J. Gould Rosemary F. Kelly Cavan S. Reilly Richard E. Isaacson Chris H. Wendt |
| author_sort | Alexa A. Pragman |
| collection | DOAJ |
| description | Abstract Background Oral taxa are often found in the chronic obstructive pulmonary disease (COPD) lung microbiota, but it is not clear if this is due to a physiologic process such as aspiration or experimental contamination at the time of specimen collection. Methods Microbiota samples were obtained from nine subjects with mild or moderate COPD by swabbing lung tissue and upper airway sites during lung lobectomy. Lung specimens were not contaminated with upper airway taxa since they were obtained surgically. The microbiota were analyzed with 16S rRNA gene qPCR and 16S rRNA gene hypervariable region 3 (V3) sequencing. Data analyses were performed using QIIME, SourceTracker, and R. Results Streptococcus was the most common genus in the oral, bronchial, and lung tissue samples, and multiple other taxa were present in both the upper and lower airways. Each subject’s own bronchial and lung tissue microbiota were more similar to each other than were the bronchial and lung tissue microbiota of two different subjects (permutation test, p = 0.0139), indicating more within-subject similarity than between-subject similarity at these two lung sites. Principal coordinate analysis of all subject samples revealed clustering by anatomic sampling site (PERMANOVA, p = 0.001), but not by subject. SourceTracker analysis found that the sources of the lung tissue microbiota were 21.1% (mean) oral microbiota, 8.7% nasal microbiota, and 70.1% unknown. An analysis using the neutral theory of community ecology revealed that the lung tissue microbiota closely reflects the bronchial, oral, and nasal microbiota (immigration parameter estimates 0.69, 0.62, and 0.74, respectively), with some evidence of ecologic drift occurring in the lung tissue. Conclusion This is the first study to evaluate the mild-moderate COPD lung tissue microbiota without potential for upper airway contamination of the lung samples. In our small study of subjects with COPD, we found oral and nasal bacteria in the lung tissue microbiota, confirming that aspiration is a source of the COPD lung microbiota. |
| first_indexed | 2024-12-14T12:29:57Z |
| format | Article |
| id | doaj.art-9d9275acd00f482c9481ff733501cbaa |
| institution | Directory Open Access Journal |
| issn | 2049-2618 |
| language | English |
| last_indexed | 2024-12-14T12:29:57Z |
| publishDate | 2018-01-01 |
| publisher | BMC |
| record_format | Article |
| series | Microbiome |
| spelling | doaj.art-9d9275acd00f482c9481ff733501cbaa2022-12-21T23:01:12ZengBMCMicrobiome2049-26182018-01-016111910.1186/s40168-017-0381-4The lung tissue microbiota of mild and moderate chronic obstructive pulmonary diseaseAlexa A. Pragman0Tianmeng Lyu1Joshua A. Baller2Trevor J. Gould3Rosemary F. Kelly4Cavan S. Reilly5Richard E. Isaacson6Chris H. Wendt7Department of Medicine, University of Minnesota and Minneapolis Veterans Affairs Medical Center, Minneapolis VA Health Care SystemDivision of Biostatistics, University of Minnesota School of Public HealthMinnesota Supercomputing Institute, University of MinnesotaBiological Science Dean’s Office, University of Minnesota Informatics InstituteDivision of Cardiothoracic Surgery, University of Minnesota and Minneapolis Veterans Affairs Medical CenterDivision of Biostatistics, University of Minnesota School of Public HealthDepartment of Veterinary and Biomedical Sciences, University of MinnesotaDepartment of Medicine, University of Minnesota and Minneapolis Veterans Affairs Medical Center, Minneapolis VA Health Care SystemAbstract Background Oral taxa are often found in the chronic obstructive pulmonary disease (COPD) lung microbiota, but it is not clear if this is due to a physiologic process such as aspiration or experimental contamination at the time of specimen collection. Methods Microbiota samples were obtained from nine subjects with mild or moderate COPD by swabbing lung tissue and upper airway sites during lung lobectomy. Lung specimens were not contaminated with upper airway taxa since they were obtained surgically. The microbiota were analyzed with 16S rRNA gene qPCR and 16S rRNA gene hypervariable region 3 (V3) sequencing. Data analyses were performed using QIIME, SourceTracker, and R. Results Streptococcus was the most common genus in the oral, bronchial, and lung tissue samples, and multiple other taxa were present in both the upper and lower airways. Each subject’s own bronchial and lung tissue microbiota were more similar to each other than were the bronchial and lung tissue microbiota of two different subjects (permutation test, p = 0.0139), indicating more within-subject similarity than between-subject similarity at these two lung sites. Principal coordinate analysis of all subject samples revealed clustering by anatomic sampling site (PERMANOVA, p = 0.001), but not by subject. SourceTracker analysis found that the sources of the lung tissue microbiota were 21.1% (mean) oral microbiota, 8.7% nasal microbiota, and 70.1% unknown. An analysis using the neutral theory of community ecology revealed that the lung tissue microbiota closely reflects the bronchial, oral, and nasal microbiota (immigration parameter estimates 0.69, 0.62, and 0.74, respectively), with some evidence of ecologic drift occurring in the lung tissue. Conclusion This is the first study to evaluate the mild-moderate COPD lung tissue microbiota without potential for upper airway contamination of the lung samples. In our small study of subjects with COPD, we found oral and nasal bacteria in the lung tissue microbiota, confirming that aspiration is a source of the COPD lung microbiota.http://link.springer.com/article/10.1186/s40168-017-0381-4RNA, Ribosomal, 16SEmigration and immigrationLungPulmonary disease, chronic obstructiveMicrobiotaStreptococcus |
| spellingShingle | Alexa A. Pragman Tianmeng Lyu Joshua A. Baller Trevor J. Gould Rosemary F. Kelly Cavan S. Reilly Richard E. Isaacson Chris H. Wendt The lung tissue microbiota of mild and moderate chronic obstructive pulmonary disease Microbiome RNA, Ribosomal, 16S Emigration and immigration Lung Pulmonary disease, chronic obstructive Microbiota Streptococcus |
| title | The lung tissue microbiota of mild and moderate chronic obstructive pulmonary disease |
| title_full | The lung tissue microbiota of mild and moderate chronic obstructive pulmonary disease |
| title_fullStr | The lung tissue microbiota of mild and moderate chronic obstructive pulmonary disease |
| title_full_unstemmed | The lung tissue microbiota of mild and moderate chronic obstructive pulmonary disease |
| title_short | The lung tissue microbiota of mild and moderate chronic obstructive pulmonary disease |
| title_sort | lung tissue microbiota of mild and moderate chronic obstructive pulmonary disease |
| topic | RNA, Ribosomal, 16S Emigration and immigration Lung Pulmonary disease, chronic obstructive Microbiota Streptococcus |
| url | http://link.springer.com/article/10.1186/s40168-017-0381-4 |
| work_keys_str_mv | AT alexaapragman thelungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT tianmenglyu thelungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT joshuaaballer thelungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT trevorjgould thelungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT rosemaryfkelly thelungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT cavansreilly thelungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT richardeisaacson thelungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT chrishwendt thelungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT alexaapragman lungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT tianmenglyu lungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT joshuaaballer lungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT trevorjgould lungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT rosemaryfkelly lungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT cavansreilly lungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT richardeisaacson lungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease AT chrishwendt lungtissuemicrobiotaofmildandmoderatechronicobstructivepulmonarydisease |