Published ahead of print on April 30, 2003, doi:10.1164/rccm.200211-1289OC Am. J. Respir. Crit. Care Med., Volume 168, Number 2, July 2003, 215-221 A more recent version of this article appeared on July 15, 2003
Submitted on November 19, 2002 Effect of diesel on chemokines and chemokine receptors involved in Th1/Th2 recruitment in asthmaticsStephanie Senechal1,1 Institute National de la Sante et de la Recherche Medicale, U-416, Institut Pasteur de Lille, Lille, France, 2 Clinique des Maladies Respiratoires et Centre Hospitalier Regional et Universitaire de Lille, Lille, France, 3 Institute National de la Sante et de la Recherche Medicale, U-416, Institut Pasteur de Lille, Lille, France; Clinique des Maladies Respiratoires et Centre Hospitalier Regional et Universitaire de Lille, Lille, France * To whom correspondence should be addressed. E-mail: anne.tsicopoulos{at}pasteur-lille.fr.
The objective of this study was to evaluate if diesel exhausts could favor Th2 associated allergic reactions either through an increased production of Th-2 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 allergic subjects 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, Th1/Th2, Allergy, Asthma.
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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 mecanism to clear pro-Th1 chemokines and promote the Th2 pathway.
