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Am. J. Respir. Crit. Care Med., Volume 164, Number 10, November 2001, 1867-1873

Induction of Inflammatory Response of Mice Exposed to Diesel Exhaust Is Modulated by CD4+ and CD8+ T Cells

HIDEKAZU FUJIMAKI, NAOYA UI, and TOMOHIKO ENDO

National Institute for Environmental Studies, Onogawa, Tsukuba, Ibaraki, Japan; and the Jikei University School of Medicine, Minato-ku, Tokyo, Japan

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/m3 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)-1beta production but decreased IL-12 production. DE exposure significantly enhanced production of the macrophage inflammatory proteins (MIP)-1alpha 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.




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