Novosphingobium and its potential role in chronic obstructive pulmonary diseases: insights from microbiome studies.
Novosphingobium and its potential role in chronic obstructive pulmonary diseases: insights from microbiome studies.
复制标题
新鞘氨醇及其在慢性阻塞性肺疾病中的潜在作用:来自微生物组研究的见解。
DOI:
10.1371/journal.pone.0111150
复制
发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Harris JK
中科院分区:
文献类型:
--
作者:
Rutebemberwa A;Stevens MJ;Perez MJ;Smith LP;Sanders L;Cosgrove G;Robertson CE;Tuder RM;Harris JK
Bacterial infection of lung airways underlies some of the main complications of COPD, significantly impacting disease progression and outcome. Colonization by bacteria may further synergize, amplify, or trigger pathways of tissue damage started by cigarette smoke, contributing to the characteristic airway inflammation and alveolar destruction of COPD. We sought to elucidate the presence and types of lung bacterial populations in different stages of COPD, aimed at revealing important insights into the pathobiology of the disease. Sequencing of the bacterial small subunit ribosomal RNA gene in 55 well-characterized clinical lung samples, revealed the presence of Novosphingobium spp. (>2% abundance) in lungs of patients with GOLD 3-GOLD 4 COPD, cystic fibrosis and a subset of control individuals. Novosphingobium-specific quantitative PCR was concordant with the sequence data and high levels of Novosphingobium spp. were quantifiable in advanced COPD, but not from other disease stages. Using a mouse model of subacute lung injury due to inhalation of cigarette smoke, bronchoalveolar lavage neutrophil and macrophage counts were significantly higher in mice challenged intratracheally with N. panipatense compared to control mice (p<0.01). Frequencies of neutrophils and macrophages in lung tissue were increased in mice challenged with N. panipatense at room air compared to controls. However, we did not observe an interaction between N. panipatense and subacute cigarette smoke exposure in the mouse. In conclusion, Novosphingobium spp. are present in more severe COPD disease, and increase inflammation in a mouse model of smoke exposure.
登录
查看更多内容
影响因子:
3.7
作者:
Erb-Downward JR;Thompson DL;Han MK;Freeman CM;McCloskey L;Schmidt LA;Young VB;Toews GB;Curtis JL;Sundaram B;Martinez FJ;Huffnagle GB
通讯作者:
Huffnagle GB
DOI:
10.1016/j.jaci.2010.10.048
发表时间:
2011-02
期刊:
The Journal of allergy and clinical immunology
影响因子:
--
作者:
Huang YJ;Nelson CE;Brodie EL;Desantis TZ;Baek MS;Liu J;Woyke T;Allgaier M;Bristow J;Wiener-Kronish JP;Sutherland ER;King TS;Icitovic N;Martin RJ;Calhoun WJ;Castro M;Denlinger LC;Dimango E;Kraft M;Peters SP;Wasserman SI;Wechsler ME;Boushey HA;Lynch SV;National Heart, Lung, and Blood Institute's Asthma Clinical Research Network
通讯作者:
National Heart, Lung, and Blood Institute's Asthma Clinical Research Network
DOI:
10.1164/rccm.201210-1913oc
发表时间:
2013-05-15
影响因子:
24.7
作者:
Morris, Alison;Beck, James M.;Weinstock, George M.
通讯作者:
Weinstock, George M.
DOI:
10.1513/pats.200707-088et
发表时间:
2008-05-01
期刊:
Proceedings of the American Thoracic Society
影响因子:
--
作者:
MacIntyre, Neil;Huang, Yuh Chin
通讯作者:
Huang, Yuh Chin
DOI:
10.1513/pats.200707-097th
发表时间:
2007-12-01
期刊:
Proceedings of the American Thoracic Society
影响因子:
--
作者:
Martinez, Fernando J
通讯作者:
Martinez, Fernando J