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Alternation of Innate and Cell-Mediated Immunity to Listeria Monocytogenes by Short-Term Exposure to Diesel Exhaust Particles.
Schafer R; Antonini JM; Barger MW; Dong C; Roberts JR; De La Rosa P; Ma JYC; Ma JKH
FASEB J 2002 Mar; 16(5):A962
The effects of diesel exhaust particles (DEP) on functions of pulmonary host defense were studied using a rat Listeria infection model. Short-term DEP inhalation (50 and 100 mg/m3, 4 h) by rats resulted in a slowed lung bacterial clearance, suppressed alveolar macrophage (AM) phagocytosis and reduced AM production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-l and IL-12 in response to Listeria. The combined DEP/Listeria exposure was also characterized by increased CD4+ and CD8+ cell counts, and percentage of CD8+ cells in lung draining lymph nodes. The lymphocytes from DEP-treated rats showed increased IL-2 production when challenged with concanavalin A (ConA). Cells from the combined exposed rats produced increased interferon (IFN)-gamma at day 7, but decreased IFN-gamma at day 3, when challenged with either ConA or heat-killed Listeria (HKLM). Listeria significantly induced lymphocyte secretion of IL-6 in response to HKLM, which could be increased by DEP preexposure. These results indicate that short-term DEP exposure aggravates Listeria infection by suppressing AM phagocytosis and the production of TNF-alpha, IL-l and IL-12, and by eliciting an adverse effect on T-cell-mediated immunity.
Diesel exhausts; Exposure levels; Tumors; Lung disorders; Pulmonary system disorders; Lymph nodes; Laboratory animals; Animal studies; Animals; Exhaust gases; Combustion gases
Abstract; Conference/Symposia Proceedings
Issue of Publication
The FASEB Journal, Experimental Biology 2002, New Orleans, Louisiana, April 20-24, 2002
Page last reviewed: March 3, 2021
Content source: National Institute for Occupational Safety and Health Education and Information Division