The lung tissue microbiota of mild and moderate chronic obstructive pulmonary disease.

The lung tissue microbiota of mild and moderate chronic obstructive pulmonary disease.
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DOI:
10.1186/s40168-017-0381-4
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发表时间:
2018-01-09
期刊:
影响因子:
15.5
通讯作者:
Wendt CH
Wendt CH
中科院分区:
生物学1区
文献类型:
--
作者:
Pragman AA;Lyu T;Baller JA;Gould TJ;Kelly RF;Reilly CS;Isaacson RE;Wendt CH

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在慢性阻塞性肺疾病(COPD)肺微生物群中经常发现口腔分类群,但尚不清楚这是否是由于生理过程,如样本采集时的吸入或实验污染。通过在肺叶切除术期间擦拭肺组织和上气道部位从患有轻度或中度COPD的9名受试者获得微生物群样品。肺标本未被上呼吸道分类群污染,因为它们是通过手术获得的。用16S rRNA基因qPCR和16S rRNA基因高变区3(V3)测序分析微生物群。使用QIIME、SourceTracker和R.链球菌是口腔、支气管和肺组织样品中最常见的属,并且在上呼吸道和下呼吸道中存在多种其他分类群。每个受试者自己的支气管和肺组织微生物群比两个不同受试者的支气管和肺组织微生物群彼此更相似(排列检验,p = 0.0139),表明在这两个肺部部位,受试者内的相似性比受试者间的相似性更大。所有受试者样本的主坐标分析显示了解剖采样部位的聚类(PERMANOVA,p = 0.001),但不是受试者的聚类。SourceTracker分析发现,肺组织微生物群的来源是21.1%(平均)口腔微生物群,8.7%鼻腔微生物群和70.1%未知。使用群落生态学中性理论的分析显示,肺组织微生物群密切反映了支气管,口腔和鼻腔微生物群(移民参数估计值分别为0.69,0.62和0.74),有一些证据表明肺组织中发生了生态漂移。这是第一项评估轻中度COPD肺组织微生物群的研究,而没有肺样本的上呼吸道污染的可能性。在我们对COPD受试者的小型研究中,我们在肺组织微生物群中发现了口腔和鼻腔细菌,证实了吸入是COPD肺微生物群的来源。
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. 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. 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. 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.
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