Alteration of Pulmonary Immunity to Listeria monocytogenes by Diesel Exhaust Particles (DEPs). I. Effects of DEPs on Early Pulmonary Responses

Details

• Personal Author:
  Antonini J ; Barger M ; Ma J ; Roberts J ; Schafer R ; Siegel P ; Weissman, David N. ; Yin X
• Description:
  It has been hypothesized that diesel exhaust particles (DEPs) aggravate pulmonary bacterial infection by both innate and cell-mediated immune mechanisms. To test this hypothesis, we investigated the effects of DEP exposure on the functions of alveolar macrophages (AMs) and lymphocytes from lung-draining lymph nodes using a rat Listeria monocytogenes infection model. In the present study, we focused on the effects of DEP exposure on AM functions, including phagocytic activity and secretion of proinflammatory cytokines. The Listeria infection model was characterized by an increase in neutrophil count, albumin content, and acellular lactate dehydrogenase activity in the bronchoalveolar lavage (BAL) fluid at 3 and 7 days postinfection. Short-term DEP inhalation (50 and 100 mg/m(3), 4 hr) resulted in a dose-dependent suppression of lung clearance of Listeria, with the highest bacteria count occurring at day 3. This aggravated bacterial infection was consistent with the inhibitory effect of DEPs on macrophage functions. DEPs suppressed phagocytosis and Listeria-induced basal secretion of interleukin-1ss (IL-1ss) and IL-12 by AMs in a dose-dependent manner. The amount of IL-1ss and IL-12 in the BAL fluid was also reduced by DEP exposure. In addition, DEPs decreased Listeria-induced lipopolysaccharide-stimulated secretion of tumor necrosis factor-alpha (TNF-alpha), IL-1ss, and IL-12 from AMs. These results suggest that DEPs retard bacterial clearance by inhibiting AM phagocytosis and weaken the innate immunity by inhibiting AM secretion of IL-1ss and TNF-alpha. DEPs may also suppress cell-mediated immunity by inhibiting AM secretion of IL-12, a key cytokine for the initiation of T helper type 1 cell development in Listeria infection. [Description provided by NIOSH]
• Subjects:
  Animals Blood Immune System Laboratories Occupational Health Respiratory System Respiratory Tract Diseases Safety Vehicle Emissions
• Keywords:
  Animal-studies Author Keywords: Alveolar Macrophages Cytokine Production Diesel-emissions Diesel-exhausts Diesel Exhaust Particles Emission-sources Humans Immunology Inhalation-studies Inhalation Exposure Laboratory-animals Listeria Monocytogenes Lymphocytes Occupational Exposure Pathogenicity Phagocytosis Pharmacology Physiology Pulmonary-system-disorders

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• ISSN:
  0091-6765
• 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
• Volume:
  110
• Issue:
  11
• NIOSHTIC Number:
  nn:20022364
• Citation:
  Environ Health Perspect 2002 Nov; 110(11):1105-1111
• Contact Point Address:
  J.K.H. Ma, School of Pharmacy, West Virginia University, P.O. Box 9530, 1 Medical Center Drive, HSC North, Morgantown, West Virginia 26506-9530, USA
• Email:
  jma@hsc.wvu.edu
• Federal Fiscal Year:
  2003
• NORA Priority Area:
  Work Environment And Workforce: Mixed Exposures
• Peer Reviewed:
  True
• Source Full Name:
  Environmental Health Perspectives
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:97b10063df78560eac980ff1ba6e9b25f89cb692b69b2dd4054a56a0a75f55e7f3795d6dfd252a3401c8f68edd84190fc90a5c2cb989dd507092a078b1235747
• Download URL:
  https://stacks.cdc.gov/view/cdc/199168/cdc_199168_DS1.pdf
• File Type:
  [PDF - 562.55 KB ]