title: Differential impact of diesel particle composition on pro-allergic dendritic cell function.
abstract: 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.
authors.affiliation: ZAUM-Center for Allergy and Environment, Technische Universität München, Division of Environmental Dermatology and Allergy, Helmholtz Zentrum München/TUM, 80802 Munich, Germany.
authors.forename: Andrea
authors.initials: A
authors.lastname: Braun
authors.forename: Mayte
authors.initials: M
authors.lastname: Bewersdorff
authors.forename: Jutta
authors.initials: J
authors.lastname: Lintelmann
authors.forename: Georg
authors.initials: G
authors.lastname: Matuschek
authors.forename: Thilo
authors.initials: T
authors.lastname: Jakob
authors.forename: Martin
authors.initials: M
authors.lastname: Göttlicher
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Schober
authors.forename: Jeroen T M
authors.initials: JT
authors.lastname: Buters
authors.forename: Heidrun
authors.initials: H
authors.lastname: Behrendt
authors.forename: Martin
authors.initials: M
authors.lastname: Mempel
mesh_terms: D000818:Animals; D000954:Antigens, Surface / Q000378:metabolism; D001402:B-Lymphocytes / Q000187:drug effects* / Q000276:immunology; D002478:Cells, Cultured; D018920:Coculture Techniques; D003713:Dendritic Cells / Q000187:drug effects* / Q000276:immunology; D004305:Dose-Response Relationship, Drug; D005260:Female; D006967:Hypersensitivity / Q000209:etiology* / Q000276:immunology; D007073:Immunoglobulin E / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D052638:Particulate Matter / Q000633:toxicity*; D010641:Phenotype; D053260:Soot / Q000633:toxicity*; D018418:Th2 Cells / Q000187:drug effects* / Q000276:immunology; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D000954:Antigens, Surface; D015850:Interleukin-6; D008070:Lipopolysaccharides; D052638:Particulate Matter; D053260:Soot; D001335:Vehicle Emissions; D016753:Interleukin-10; D018664:Interleukin-12; D007073:Immunoglobulin E