Diesel Exhaust and its Impact on the Allergic Response
Diesel Exhaust and its Impact on the Allergic Response
Chang Y, Senechal S, de Nadai P, et al
J Allergy Clin Immunol. 2006;118:354-360
The aim of this study was to test the hypothesis that diesel exhaust exposure might favor the recruitment of TH2 lymphocytes in nonatopic donors, either through increased production of TH2-attracting chemokines or decreased production of TH1-attracting chemokines.
Type 2 T helper cells (TH2) have been associated with allergic diseases such as asthma and allergic rhinitis, whereas type 1 T helper cells (TH1) have been more closely associated with autoimmune diseases. It has been postulated that exposure to various air pollutants may not only amplify the allergic response in those who already have an allergic predisposition, but also may in fact help initiate allergic sensitivity in those who were previously nonatopic. Chang and colleagues incubated peripheral blood mononuclear cells with diesel exhaust particle-polyaromatic hydrocarbons and analyzed the supernatants for evidence of pro-TH1 and pro-TH2 chemokines. The end result of this experiment was an enhanced chemotaxis of TH2, but not TH1 cells.
The study authors point out that these findings suggest that diesel exhaust particulates not only might be involved in enhancing IgE production and the allergic response to allergens in those already allergic, but that they also could be important in the genesis of allergic sensitivity in those who were previously nonatopic. Perhaps we should be paying more attention to the emissions of diesel vehicles than we are currently.
Abstract
Chang Y, Senechal S, de Nadai P, et al
J Allergy Clin Immunol. 2006;118:354-360
The aim of this study was to test the hypothesis that diesel exhaust exposure might favor the recruitment of TH2 lymphocytes in nonatopic donors, either through increased production of TH2-attracting chemokines or decreased production of TH1-attracting chemokines.
Type 2 T helper cells (TH2) have been associated with allergic diseases such as asthma and allergic rhinitis, whereas type 1 T helper cells (TH1) have been more closely associated with autoimmune diseases. It has been postulated that exposure to various air pollutants may not only amplify the allergic response in those who already have an allergic predisposition, but also may in fact help initiate allergic sensitivity in those who were previously nonatopic. Chang and colleagues incubated peripheral blood mononuclear cells with diesel exhaust particle-polyaromatic hydrocarbons and analyzed the supernatants for evidence of pro-TH1 and pro-TH2 chemokines. The end result of this experiment was an enhanced chemotaxis of TH2, but not TH1 cells.
The study authors point out that these findings suggest that diesel exhaust particulates not only might be involved in enhancing IgE production and the allergic response to allergens in those already allergic, but that they also could be important in the genesis of allergic sensitivity in those who were previously nonatopic. Perhaps we should be paying more attention to the emissions of diesel vehicles than we are currently.
Abstract
