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Am J Physiol Lung Cell Mol Physiol (March 5, 2004). doi:10.1152/ajplung.00290.2003
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Submitted on August 26, 2003
Accepted on March 2, 2004

The contribution of IL-1{beta} and TNF-{alpha} to the initiation of the peripheral lung response to atmospheric particulates (PM10)

Hiroshi Ishii1, Takeshi Fujii1, James C. Hogg1, Shizu Hayashi1, Hiroshi Mukae1, Renaud Vincent2, and Stephan F. van Eeden1*

1 James Hogg iCAPTURE Centre for cardiovascular and pulmonary research, St. Paul's Hospital, University of British Columbia, Vancouver, British Columbia, Canada
2 Environmental Health Directorate, Health Canada, Ottawa, Ontario, Canada

* To whom correspondence should be addressed. E-mail: SVaneeden{at}mrl.ubc.ca.

Alveolar macrophages (AM) play a key role in clearing atmospheric particulates from the lung surface and stimulating epithelial cells to produce pro-inflammatory mediators. The present study examines the role of "acute response" cytokines TNF-{alpha} and IL-1{beta} released by AM exposed to ambient PM10 in amplifying the pro-inflammatory mediator expression by A549 cells and human bronchial epithelial cells (HBEC). The results showed that supernatants from human AM incubated 24 h with PM10 (100 µg/ml) contained more TNF{alpha}, IL-1{beta}, granulocyte-macrophage colony stimulating factor, IL-6 and IL-8 than nonexposed AM supernatants. The 3 h treatment of A549 cells with PM10-exposed AM supernatants increased TNF-{alpha}, IL-1{beta}, IL-8, regulated on activation normal T-cells expressed and secreted (RANTES) and leukemia inhibitory factor mRNA compared to the treatment with non-exposed AM supernatants and, compared to untreated A549 cells, additionally increased ICAM-1 and monocyte chemotactic protein-1 mRNA. Preincubating PM10-exposed AM supernatants with anti-IL-1{beta} antibodies reduced all the above mediators as well as VEGF mRNA expression (p<0.05) while anti-TNF-{alpha} antibodies were less effective (p>0.05) and the combination of the two antibodies, most effective. When HBEC were treated similarly anti-TNF-{alpha} antibodies had the greatest effect. In A549 cells PM10- exposed AM supernatants increased NF-{kappa}B, activator protein (AP)-1 and specificity protein 1 binding while anti-TNF-{alpha} and anti-IL-1{beta} antibodies reduced NF-{kappa}B and AP-1 binding. We conclude that AM-derived TNF-{alpha} and IL-1{beta} provide a major stimulus for the production of pro-inflammatory mediators by lung epithelial cells and that their relative importance may depend on the type of epithelial cell target.




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