Diesel exhaust exposure favors TH2 cell recruitment in nonatopic subjects by differentially regulating chemokine production

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The prevalence of allergic diseases has increased in the last 20 years, and a number of studies have shown that diesel exhaust particle–associated polyaromatic hydrocarbons can exacerbate the allergic reaction. Much less is known about their potential capacity to generate a TH2-type allergic reaction in nonatopic subjects.


The aim of this study was to test the hypothesis that diesel exhaust exposure might favor, in nonatopic donors, TH2-type cell recruitment, either through increased production of TH2-attracting chemokines or decreased production of TH1-attracting chemokines.


PBMCs from nonatopic donors were incubated with diesel exhaust particle–polyaromatic hydrocarbons, and the supernatants were evaluated for the presence of pro-TH1 chemokines (IFN-γ–induced protein 10 and monokine Induced by IFN-γ) and pro-TH2 chemokines (macrophage-derived chemokine, I-309, and pulmonary and activation-regulated chemokine) by means of ELISA. The functional effect was evaluated by using chemotaxis assays with polarized TH1 and TH2 cells.


Diesel exhaust exposure of PBMCs from nonatopic donors induced a late increase after 48 hours in pulmonary and activation-regulated chemokine mediated by IL-13 and a decrease in IFN-γ–induced protein 10 levels selectively at both the protein and mRNA levels. The functional effect of these chemokine variations resulted in an enhanced chemotaxis of TH2, but not TH1, cells.


These findings show that diesel exhaust exposure might be involved in the genesis of allergic diseases by differentially regulating chemokines favoring the recruitment of TH2 cells in nonatopic subjects.

Clinical implications

Environmental factors, especially air pollution, might favor the genesis of allergic diseases.

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