EVALUATION OF INFLAMMATORY EFFECTS OF AIRBORNE ENDOTOXIN EMITTED FROM COMPOSTING SOURCES

被引：11

作者：

Liu, Jian ^{[2
]}

Pankhurst, Louise J. ^{[3
]}

Deacon, Lewis J. ^{[3
]}

Abate, Wondwossen ^{[1
]}

Hayes, Enda T. ^{[2
]}

Drew, Gill H. ^{[3
]}

Longhurst, Phil J. ^{[3
]}

Pollard, Simon ^{[3
]}

Longhurst, James ^{[2
]}

Tyrrel, Sean F. ^{[3
]}

Jackson, Simon K. ^{[1
]}

机构：

[1] Univ Plymouth, Plymouth PL4 8AA, Devon, England

[2] Univ W England, Bristol BS16 1QY, Avon, England

[3] Cranfield Univ, Cranfield MK43 0AL, Beds, England

来源：

ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY | 2011年 / 30卷 / 03期

基金：

英国自然环境研究理事会;

关键词：

Endotoxin; Composting; In vitro; Cytokine; BURKHOLDERIA-CEPACIA; CYTOKINE RESPONSES; ORGANIC DUST; EXPOSURE; LIPOPOLYSACCHARIDES; WORKERS; RELEASE; PLANTS;

D O I：

10.1002/etc.434

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

Because of the lack of effective methodology, the biological effects of environmental endotoxin have not been assessed. Here we have collected and measured airborne endotoxin at different locations around composting sites. Increased endotoxin concentrations were observed close to composting activities and also at nearby boundary areas. Analysis of proinflammatory effects of the environmental endotoxin on interleukin (IL)-8 and IL-6 release from human 0562 pharyngeal epithelial and MM6 monocytic cell cultures showed an association between endotoxin level and cytokine induction. The cytolcine-inducing effect of bioaerosol extracts was inhibited by polymyxin B, indicating that endotoxin was the cause of cytokine responses we found. The environmental endotoxin was also more active for stimulating cytokines in airway epithelial cells than commercially purified Escherichia coli endotoxin. Our results suggest that these in vitro inflammatory cell models may contribute to the assessment of health impacts of environmental endotoxin. Environ. Toxicol. Chem. 2011;30:602-606. (C) 2011 SETAC

引用

页码：602 / 606

页数：5

共 24 条

[1] Highly purified lipopolysaccharides from Burkholderia cepacia complex clinical isolates induce inflammatory cytokine responses via TLR4-mediated MAPK signalling pathways and activation of NFκB [J].