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Differential Impact of Diesel Particle Composition on Pro-allergic Dendritic Cell Function
Author(s) -
Andrea Braun,
Mayte Bewersdorff,
Jutta Lintelmann,
G. Matuschek,
Thilo Jakob,
Martin Göttlicher,
Wolfgang Schöber,
Jeroen Buters,
Heidrun Behrendt,
Martin Mempel
Publication year - 2009
Publication title -
toxicological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.352
H-Index - 183
eISSN - 1096-6080
pISSN - 1096-0929
DOI - 10.1093/toxsci/kfp239
Subject(s) - dendritic cell , immune system , immunoglobulin class switching , immunology , isotype , microbiology and biotechnology , cytokine , lipopolysaccharide , chemistry , immunoglobulin e , biology , antibody , b cell , monoclonal antibody
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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