Diesel exhaust exposure favors TH2 cell recruitment in nonatopic subjects by differentially regulating chemokine production.
BACKGROUND
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 T(H)2-type allergic reaction in nonatopic subjects.


OBJECTIVE
The aim of this study was to test the hypothesis that diesel exhaust exposure might favor, in nonatopic donors, T(H)2-type cell recruitment, either through increased production of T(H)2-attracting chemokines or decreased production of T(H)1-attracting chemokines.


METHODS
PBMCs from nonatopic donors were incubated with diesel exhaust particle-polyaromatic hydrocarbons, and the supernatants were evaluated for the presence of pro-T(H)1 chemokines (IFN-gamma-induced protein 10 and monokine Induced by IFN-gamma) and pro-T(H)2 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 T(H)1 and T(H)2 cells.


RESULTS
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-gamma-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 T(H)2, but not T(H)1, cells.


CONCLUSIONS
These findings show that diesel exhaust exposure might be involved in the genesis of allergic diseases by differentially regulating chemokines favoring the recruitment of T(H)2 cells in nonatopic subjects.


CONCLUSIONS
Environmental factors, especially air pollution, might favor the genesis of allergic diseases.
Chang
Ying
Y
INSERM U-774, Institut Pasteur de Lille, 59 019 Lille Cedex, France.
Sénéchal
Stéphanie
S
de Nadai
Patricia
P
Chenivesse
Cécile
C
Gilet
Jules
J
Vorng
Han
H
Legendre
Benjamin
B
Tonnel
André-Bernard
AB
Wallaert
Benoît
B
Lassalle
Philippe
P
Tsicopoulos
Anne
A
D000328:Adult; D002478:Cells, Cultured; D018925:Chemokines / Q000096:biosynthesis; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology* / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D008875:Middle Aged; D011084:Polycyclic Aromatic Hydrocarbons / Q000633:toxicity*; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology; D018418:Th2 Cells / Q000187:drug effects* / Q000276:immunology; D001335:Vehicle Emissions / Q000633:toxicity*
D018925:Chemokines; D011084:Polycyclic Aromatic Hydrocarbons; D001335:Vehicle Emissions