title: Induction of inflammatory response of mice exposed to diesel exhaust is modulated by CD4(+) and CD8(+) T cells.
abstract: Exposure to diesel exhaust (DE) increased airway inflammatory responses and airway responsiveness to allergen challenge. To clarify the roles of T cells in DE exposure-induced early inflammation, we studied the effect of CD4 and CD8 cells on the effect DE might have on allergic inflammation by using monoclonal antibody-mediated cellular depletion assays. In the bronchoalveolar lavage (BAL) fluid, the numbers of inflammatory cells from 3 mg/m(3) DE-exposed and ovalbumin (OVA)-immunized mice markedly increased. Depletion of CD4(+) cells resulted in reduced accumulation of inflammatory cells. DE exposure to OVA-immunized mice significantly increased interleukin (IL)-1 beta production but decreased IL-12 production. DE exposure significantly enhanced production of the macrophage inflammatory proteins (MIP)-1 alpha and MIP-2, but not monocyte chemoattractant protein (MCP)-1 and regulated upon activation normal T cells expressed and secreted (RANTES). Treatment with anti-CD4 and anti-CD8 mAbs abrogated the adverse effect of DE exposure. In CLN cells from OVA + DE-exposed mice, CD45R/B220-, CD3-, CD4-, and CD8-positive cells were significantly increased, but the OVA-stimulated cytokine production remained at the same levels with OVA-immunized mice. These findings suggest that the induction of early inflammatory responses by DE exposure may initially be related to the modulated function of lymphocyte subpopulations.
authors.affiliation: National Institute for Environmental Studies, Onogawa, Tsukuba, Ibaraki, Japan. fujimaki@nies.go.jp
authors.forename: H
authors.initials: H
authors.lastname: Fujimaki
authors.forename: N
authors.initials: N
authors.lastname: Ui
authors.forename: T
authors.initials: T
authors.lastname: Endo
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000627:therapeutic use; D016535:Bronchial Hyperreactivity / Q000097:blood / Q000209:etiology* / Q000276:immunology* / Q000628:therapy; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D018932:Chemokine CCL2 / Q000276:immunology; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000276:immunology; D054426:Chemokine CXCL2; D018925:Chemokines / Q000276:immunology; D004195:Disease Models, Animal; D007114:Immunization / Q000379:methods; D016130:Immunophenotyping; D007249:Inflammation; D019570:Inhalation Exposure / Q000009:adverse effects*; D007375:Interleukin-1 / Q000276:immunology; D018664:Interleukin-12 / Q000276:immunology; D018655:Lymphocyte Count; D019402:Macrophage Inflammatory Proteins / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D013997:Time Factors; D001335:Vehicle Emissions / Q000009:adverse effects*
chemical_list: D000911:Antibodies, Monoclonal; D018932:Chemokine CCL2; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D054426:Chemokine CXCL2; D018925:Chemokines; C404915:Cxcl2 protein, mouse; D007375:Interleukin-1; D019402:Macrophage Inflammatory Proteins; D001335:Vehicle Emissions; D018664:Interleukin-12; D010047:Ovalbumin