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Contribution of IL-1 and TNF- to the initiation of the peripheral lung response to atmospheric particulates (PM₁₀)

¹James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, St. Paul's Hospital, University of British Columbia, Vancouver, British Columbia V6Z 1Y6; and ²Environmental Health Directorate, Health Canada, Ottawa, Ontario K1A 0L2, Canada

Submitted 26 August 2003 ; accepted in final form 2 March 2004

Alveolar macrophages (AM) play a key role in clearing atmospheric particulates from the lung surface and stimulating epithelial cells to produce proinflammatory mediators. The present study examines the role of "acute response" cytokines TNF- and IL-1 released by AM exposed to ambient particulate matter with a diameter of <10 µm (PM₁₀) in amplifying the proinflammatory 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-, IL-1, 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-, IL-1, IL-8, regulated on activation normal T-cells expressed and secreted (RANTES), and leukemia inhibitory factor mRNA compared with the treatment with nonexposed AM supernatants and, compared with untreated A549 cells, additionally increased ICAM-1 and monocyte chemotactic protein-1 mRNA. Preincubating PM₁₀-exposed AM supernatants with anti-IL-1 antibodies reduced all the above mediators as well as VEGF mRNA expression (P < 0.05), while anti-TNF- antibodies were less effective (P > 0.05), and the combination of the two antibodies most effective. When HBEC were treated similarly, anti-TNF- antibodies had the greatest effect. In A549 cells PM₁₀-exposed AM supernatants increased NF-B, activator protein (AP)-1 and specificity protein 1 binding, while anti-TNF- and anti-IL-1 antibodies reduced NF-B and AP-1 binding. We conclude that AM-derived TNF- and IL-1 provide a major stimulus for the production of proinflammatory mediators by lung epithelial cells and that their relative importance may depend on the type of epithelial cell target.

ribonuclease protection assay; transcription factors; enzyme-linked immunosorbent assay; proinflammatory mediators; particulate matter with diameter < 10 µm

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