Published ahead of print on April 30, 2003, doi:10.1164/rccm.200211-1289OC
© 2003 American Thoracic Society
Effect of Diesel on Chemokines and Chemokine Receptors Involved in Helper T Cell Type 1/Type 2 Recruitment in Patients with AsthmaINSERM U-416, Institut Pasteur de Lille; and Clinique des Maladies Respiratoires et Centre Hospitalier Régional et Universitaire de Lille, Lille, France Correspondence and requests for reprints should be addressed to Anne Tsicopoulos, M.D., U-416, Institut Pasteur de Lille, BP 245, 59 019 Lille Cedex, France. E-mail: anne.tsicopoulos{at}pasteur-lille.fr
The objective of this study was to evaluate if diesel exhausts could favor helper T cell type (Th) 2-associated allergic reactions either through an increased production of Th2-associated chemokines and of their associated receptors or through a decrease of Th1-attracting chemokines and chemokine receptors. Diesel but not allergen exposure of peripheral blood mononuclear cells from subjects with allergy induced a release of I-309, whereas both diesel and Der p 1 induced an early but transient release of monokine induced by IFN-
Key Words: chemokines • diesel • helper T cell type 1/type 2 • allergy • asthma This article has been cited by other articles:
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and a late release of pulmonary and activation–regulated chemokine. Although both Th1- and Th2-attracting chemokines were induced, the resulting effect was an increased chemotactic activity on Th2 but not Th1 cells. Surprisingly, diesel induced a late increase in the expression of the Th1-associated CXC receptor 3 and CC receptor 5. T cell CXC receptor 3 upregulation was not associated with an increased migration to its ligands. These two antagonistic effects have been previously reported as a scavenger mechanism to clear chemokines. Altogether, these results suggest that diesel, even without allergen, may amplify a type 2 immune response but that it can also increase late Th1-associated chemokine receptor expression, perhaps as a scavenger mechanism to clear pro-Th1 chemokines and promote the Th2 pathway. 
