Enhanced nasal cytokine production in human beings after in vivo challenge with diesel exhaust particles

Background: Diesel exhaust particles (DEPs) have been implicated in the worldwide increased incidence of allergic airway disorders over the past century. They can enhance in vivo IgE production in the human upper respiratory mucosa. Objective: The study was carried out to determine whether DEPs can...

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Veröffentlicht in:Journal of allergy and clinical immunology 1996-07, Vol.98 (1), p.114-123
Hauptverfasser: Diaz-Sanchez, David, Tsien, Albert, Casillas, Adrian, Dotson, Anton Robert, Saxon, Andrew
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Sprache:eng
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Zusammenfassung:Background: Diesel exhaust particles (DEPs) have been implicated in the worldwide increased incidence of allergic airway disorders over the past century. They can enhance in vivo IgE production in the human upper respiratory mucosa. Objective: The study was carried out to determine whether DEPs can alter the production of cytokines by cells residing in the nasal mucosa. Methods: Eighteen hours after intranasal challenge with saline solution or DEPs, we studied the levels of messenger RNA for cytokines in nasal lavage cells and the number of subjects in whom cytokine mRNA could be detected. Results: Before challenge, most subjects’ nasal lavage cells had detectable levels of only interferon-γ, IL-2, and IL-13 mRNA. After challenge, the cells produced readily detectable mRNA for IL-2, IL-4, IL-5, IL-6, IL-10, IL-13, and interferon-γ. In addition, the levels of all cytokine mRNA increased. Enhanced IL-4 protein was also present in the postchallenge lavage fluid. Although the cells in nasal lavage before and after challenge do not necessarily represent the same cells either in number or type, the broad increase in cytokine production was not simply the result of an increase in T cells recovered in the lavage fluid. Conclusion: An increase in nasal cytokine expression after exposure to DEPs can be predicted to contribute to enhanced local IgE production and thus play a role in the increased incidence of respiratory allergic disease. (J A LLERGY C LIN I MMUNOL 1996;98:114-23.)
ISSN:0091-6749
1097-6825
DOI:10.1016/S0091-6749(96)70233-6