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Braun, A. ; Bewersdorff, M. ; Lintelmann, J. ; Matuschek, G. ; Jakob, T.* ; Göttlicher, M. ; Schober, W. ; Buters, J.T.M. ; Behrendt, H. ; Mempel, M.

Differential impact of diesel particle composition on pro-allergic dendritic cell function.

Toxicol. Sci. 113, 85-94 (2010)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Diesel exhaust particles (DEP) were described as potent adjuvant in the induction and maintenance of allergic diseases, suggesting that they might play a role in the increase of allergic diseases in the industrialized countries. However, the cellular basis by which these particles enhance allergic immune responses is still a matter of debate. Thus, we exposed immature murine bone marrow-derived dendritic cells (BMDC) to different particles or particle-associated organic compounds in the absence or presence of the maturation stimuli lipopolysaccharide (LPS) and analyzed the cellular maturation, viability, and cytokine production. Furthermore, we monitored the functionality of particle-exposed BMDC to suppress B cell isotype switching to immunoglobulin (Ig) E. Only highly polluted DEP (standard reference material 1650a [SRM1650a]) but not particle-associated organic compounds or less polluted DEP from modern diesel engines were able to modulate the dendritic cell phenotype. SRM1650a particles significantly suppressed LPS-induced IL-12p70 production in murine BMDC, whereas cell-surface marker expression was not altered. Furthermore, SRM1650a-exposed immature BMDC lost the ability to suppress IgE isotype switch in B cells. This study revealed that highly polluted DEP not only interfere with dendritic cell maturation but also additionally with dendritic cell function, thus suggesting a role in T(h)2 immune deviation.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Dendritic cells; B cells; IgE; Particles; Organic compounds
ISSN (print) / ISBN 1096-6080
e-ISSN 1096-0929
Zeitschrift Toxicological Sciences
Quellenangaben Band: 113, Heft: 1, Seiten: 85-94 Artikelnummer: , Supplement: ,
Verlag Oxford University Press
Verlagsort Oxford
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) CCG Environmental Dermatology and Allergology (ILBD-KAU)
Institute of Epidemiology (EPI)
Institute of Ecological Chemistry (IOEC)
Institute of Molecular Toxicology and Pharmacology (TOXI)
Cooperation Group Comprehensive Molecular Analytics (CMA)