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Toxicological Sciences 69, 210-216 (2002)
Copyright © 2002 by the Society of Toxicology

RESPIRATORY TOXICOLOGY

Activation of Human Epithelial Lung A549 Cells by the Pollutant Sodium Sulfite: Enhancement of Neutrophil Adhesion

Martin Pelletier, Valérie Lavastre and Denis Girard1

INRS-Institut Armand-Frappier, Université du Québec, 245 Boulevard Hymus, Pointe-Claire, Québec, Canada H9R 1G6

Air pollutant exposure may induce deterioration of respiratory health. Concentrations of air particles, ozone, nitrogen dioxide, sulfur dioxide, and sulfate are among the players involved in the initiation and/or exacerbation of lung diseases. We have previously documented that the pollutant sodium sulfite (Na2SO3) is a human neutrophil agonist. To date, there is no evidence in the literature that Na2SO3 can activate epithelial lung cells. In the present study, we found that Na2SO3 (0.01–10 mM) induces tyrosine phosphorylation events and interleukin-8 production in human epithelial lung A549 cells. In addition, we found that Na2SO3 did not promote A549 cell apoptosis as assessed by the degradation of the cytoskeletal gelsolin protein and by FITC-annexin-V binding. Human neutrophil adhesion to Na2SO3-induced A549 cells was increased when compared with untreated A549 cells. As assessed by flow cytometry, cell surface expression of intercellular adhesion molecule (ICAM)-1, ICAM-3, and vascular cell adhesion molecule-1 (VCAM-1) on A549 cells was not affected by Na2SO3. We conclude that Na2SO3 can activate A549 cells. In addition, we conclude that neutrophil adhesion to Na2SO3-induced A549 cells is increased via an ICAM-1-, ICAM-3-, and VCAM-1-independent mechanism.

Key Words: inflammation; sodium sulfite; Na2SO3; lung cells; neutrophils; cell adhesion.


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