Sustained Effect of Inhaled Diesel Exhaust Particles on T-Lymphocyte-Mediated Immune Responses Against Listeria monocytogenes

Details

• Personal Author:
  Antonini JM ; Barger MW ; Dong CC ; Ma JKH ; Ma JYC ; Roberts, Jennifer R. ; Yin XJ
• Description:
  Studies have shown that exposure to diesel exhaust particles (DEP) suppresses pulmonary host defense against bacterial infection. The present study was carried out to characterize whether DEP exposure exerts a sustained effect in which inhaled DEP increase the susceptibility of the lung to bacterial infection occurring at a later time. Brown Norway rats were exposed to filtered air or DEP by inhalation at a dose of 21.2 +/- 2.3 mg/m(3), 4 h/day for 5 days, and intratracheally instilled with saline or 100,000 Listeria monocytogenes (Listeria) 7 days after the final DEP exposure. Bacterial growth and cellular responses to DEP and Listeria exposures were examined at 3 and 7 days post-infection. The results showed that inhaled DEP prolonged the growth of bacteria, administered 7 days post DEP exposure, in the lung as compared to the air-exposed controls. Pulmonary responses to Listeria infection were characterized by increased production of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, IL-12, and IL-10 by alveolar macrophages (AM) and increased presence of T lymphocytes and their CD4(+) and CD8(+) subsets in lung draining lymph nodes that secreted elevated levels of IL-2, IL-6, IL-10, and interferon (IFN)-gamma. Diesel exhaust particles were found to inhibit Listeria-induced production of IL-1beta and TNF-alpha, which are responsible for the innate immunity, and IL-12, which initiates the development of T helper (Th)1 responses, but enhance Listeria-induced AM production of IL-10, which prolongs Listeria survival in these phagocytes. The dual action of DEP on AM production of IL-12 and IL-10 correlated with an inhibition of the development of bacteria-specific T lymphocytes by DEP. Cytokine production by lymphocytes from DEP- and Listeria-exposed rats showed a marked decrease in the production of IL-2, IL-10, and IFN-gamma compared to Listeria infection alone, suggesting either that DEP inhibit the production of cytokines by lymphocytes or that these lymphocytes contained T-cell subsets that are different from those of Listeria infection alone and less effective in mediating Th1 immune responses. This study demonstrates that inhaled DEP, after a 7-day resting period, increase the susceptibility of the lung to bacterial infection occurring at a later time by inhibiting macrophage immune function and suppressing the development of T-cell-mediated immune responses. The results support the epidemiological observations that exposure to DEP may be responsible for the pulmonary health effects on humans. [Description provided by NIOSH]
• Subjects:
  Animals Bacterial Infections Environmental Monitoring Immune System Laboratories Lung Occupational Health Respiratory System Respiratory Tract Diseases Safety Vehicle Emissions

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• Keywords:
  Animal-studies Bacteria Bacterial-infections Cellular-reactions Diesel-exhausts Exposure-assessment Exposure-levels Immune-reaction Laboratory-animals Lung-irritants Pulmonary-system-disorders Respiratory-system-disorders

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• ISSN:
  1096-6080
• Document Type:
  Text
• Genre:
  Journal Article
• Place as Subject:
  OSHA Region 3 ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Pages in Document:
  73-81
• Volume:
  88
• Issue:
  1
• NIOSHTIC Number:
  nn:20028657
• Citation:
  Toxicol Sci 2005 Nov; 88(1):73-81
• Federal Fiscal Year:
  2006
• Peer Reviewed:
  True
• Source Full Name:
  Toxicological Sciences
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:2942eb256df1b3eabd9bea262db386654ad752b762007864afc6afc06e041115ff566bf1e4f9680aa5148a9422986a97522a2b90aca58c8f172aefaf1b95d616
• Download URL:
  https://stacks.cdc.gov/view/cdc/189873/cdc_189873_DS1.pdf
• File Type:
  [PDF - 287.34 KB ]