Comparative airway inflammatory response of normal volunteers to ozone and lipopolysaccharide challenge.
Comparative airway inflammatory response of normal volunteers to ozone and lipopolysaccharide challenge.
复制标题
DOI:
10.3109/08958371003610966
复制
发表时间:
2010-07
影响因子:
2.1
通讯作者:
Peden DB
中科院分区:
文献类型:
--
作者:
Hernandez ML;Harris B;Lay JC;Bromberg PA;Diaz-Sanchez D;Devlin RB;Kleeberger SR;Alexis NE;Peden DB
Ozone and lipopolysaccharide (LPS) are environmental pollutants with adverse health effects noted in both healthy and asthmatic individuals. The authors and others have shown that inhalation of ozone and LPS both induce airway neutrophilia. Based on these similarities, the authors tested the hypothesis that common biological factors determine response to these two different agents. Fifteen healthy, nonasthmatic volunteers underwent a 0.4 part per million ozone exposure for 2 h while performing intermittent moderate exercise. These same subjects underwent an inhaled LPS challenge with 20,000 LPS units of Clinical Center Reference LPS, with a minimum of 1 month separating these two challenge sessions. Induced sputum was obtained 24 h before and 4–6 h after each exposure session. Sputum was assessed for total and differential cell counts and expression of cell surface proteins as measured by flow cytometry. Sputum supernatants were assayed for cytokine concentration. Both ozone and LPS challenge augmented sputum neutrophils and subjects’ responses were significantly correlated (R = .73) with each other. Ozone had greater overall influence on cell surface proteins by modifying both monocytes (CD14, human leukocyte antigen [HLA]-DR, CD11b) and macrophages (CD11b, HLA-DR) versus LPS where CD14 and HLA-DR were modified only on monocytes. However, LPS significantly increased interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, with no significant increases seen after ozone challenge. Ozone and LPS exposure in healthy volunteers induce similar neutrophil responses in the airways; however, downstream activation of innate immune responses differ, suggesting that oxidant versus bacterial air pollutants may be mediated by different mechanisms.
登录
查看更多内容
影响因子:
14.2
作者:
Alexis, NE;Lay, JC;Becker, S
通讯作者:
Becker, S
影响因子:
3.8
作者:
Devlin, RB;McDonnell, WF;Koren, HS
通讯作者:
Koren, HS
DOI:
10.1164/rccm.200509-1424oc
发表时间:
2006-12-15
影响因子:
24.7
作者:
Gilliland, Frank D.;Li, Yu-Fen;Diaz-Sanchez, David
通讯作者:
Diaz-Sanchez, David
影响因子:
4.8
作者:
Garantziotis, Stavros;Li, Zhuowei;Hollingsworth, John W.
通讯作者:
Hollingsworth, John W.
DOI:
10.1164/rccm.2112064
发表时间:
2002-08-15
影响因子:
24.7
作者:
Gilliland, FD;Li, YF;Peters, JM
通讯作者:
Peters, JM