Diesel exhaust particle exposure in vitro alters monocyte differentiation and function.
Diesel exhaust particle exposure in vitro alters monocyte differentiation and function.
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DOI:
10.1371/journal.pone.0051107
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Sabroe I
中科院分区:
文献类型:
--
作者:
Chaudhuri N;Jary H;Lea S;Khan N;Piddock KC;Dockrell DH;Donaldson K;Duffin R;Singh D;Parker LC;Sabroe I
Air pollution by diesel exhaust particles is associated with elevated mortality and increased hospital admissions in individuals with respiratory diseases such as asthma and chronic obstructive pulmonary disease. During active inflammation monocytes are recruited to the airways and can replace resident alveolar macrophages. We therefore investigated whether chronic fourteen day exposure to low concentrations of diesel exhaust particles can alter the phenotype and function of monocytes from healthy individuals and those with chronic obstructive pulmonary disease. Monocytes were purified from the blood of healthy individuals and people with a diagnosis of chronic obstructive pulmonary disease. Monocyte-derived macrophages were generated in the presence or absence of diesel exhaust particles and their phenotypes studied through investigation of their lifespan, cytokine generation in response to Toll like receptor agonists and heat killed bacteria, and expression of surface markers. Chronic fourteen day exposure of monocyte-derived macrophages to concentrations of diesel exhaust particles >10 µg/ml caused mitochondrial and lysosomal dysfunction, and a gradual loss of cells over time both in healthy and chronic obstructive pulmonary disease individuals. Chronic exposure to lower concentrations of diesel exhaust particles impaired CXCL8 cytokine responses to lipopolysaccharide and heat killed E. coli, and this phenotype was associated with a reduction in CD14 and CD11b expression. Chronic diesel exhaust particle exposure may therefore alter both numbers and function of lung macrophages differentiating from locally recruited monocytes in the lungs of healthy people and patients with chronic obstructive pulmonary disease.
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DOI:
10.1165/ajrcmb.23.4.3959
发表时间:
2000-10-01
影响因子:
6.4
作者:
Rusznak, C;Mills, PR;Lozewicz, S
通讯作者:
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影响因子:
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作者:
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影响因子:
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影响因子:
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作者:
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通讯作者:
van Eeden SF
DOI:
10.1164/rccm.200402-235oc
发表时间:
2004-10-15
影响因子:
24.7
作者:
Goto, Y;Ishii, H;van Eeden, SF
通讯作者:
van Eeden, SF