Effects of Vanadium upon polyl:C-Induced Responses in Rat Lung and Alveolar Macrophages

Details

• Personal Author:
  Becker S ; Cohen MD ; Devlin R ; Schlesinger RB ; Zelikoff JT ; Becker S ; Cohen MD ; Devlin R ; Schlesinger RB ; Zelikoff JT
• Description:
  Hosts exposed to vanadium (V) display a subsequent decrease in their resistance to infectious microorganisms. Our earlier studies with rats inhaling occupationally relevant levels of V (as, ammonium metavanadate, NH4VO3) indicated that several nascent/inducible functions of pulmonary macrophages (PAM) were reduced. In the present study, V-exposed rats were examined to determine whether some of the same effects might also occur in situ. Rats were exposed nose-only to air or 2 mg V/m3 (as NH4VO3) for 8 h/d for 4 d, followed, 24 h later, by intratracheal (it) instillation of polyinosinic:polycytidilic acid (polyl:C) or saline. Analysis of lavaged lung cells/fluids after polyl:C instillation indicated that total lavageable cell/neutrophil numbers and protein levels, while significantly elevated in both exposure groups (as well as in saline-treated V-exposed rats), were always greater in V-exposed hosts. Exposure to V also affected the inducible production of interleukin 6 (IL-6) and interferon gamma (IFN gamma), but apparently not that of tumor necrosis factor-alpha (TNF alpha) or IL-1. Although polyl:C induced significant increases in lavage fluid IL-6 and IFN gamma levels in both exposure groups, levels were greater in V-exposed rats. If calculated with respect to total lavaged protein, however, V-exposed rats produced significantly less cytokine. Following polyl:C instillation, there were no marked exposure-related differences in basal or stimulated superoxide anion production by pooled lavaged cells or PAM specifically. With V-exposed rats, pooled cells recovered 24 h after saline instillation displayed reduced production (in both cases) compared to the air control cells; PAM-specific production was affected only after stimulation. In both exposure groups, polyl:C caused decreased superoxide production in recovered cells. Though less apparent with pooled cells, there was a time post polyl:C instillation-dependent decrease in stimulated PAM-specific superoxide production; this effect was greater in PAM from V-exposed rats than in PAM from air controls. Phagocytic activity of PAM from rats in both exposure groups was significantly increased by polyl:C instillation, although total activity in cells obtained from V-exposed rats was always significantly lower compared to air control cells. Our results indicate that short-term, repeated inhalation of occupationally relevant levels of V by rats modulates pulmonary immunocompetence. Modified cytokine production and PAM functionality in response to biological response modifiers (such as lipopolysaccharide, IFN gamma, or polyl:C) may be, at least in part, responsible for the increases in bronchopulmonary disease in humans occupationally exposed to V. [Description provided by NIOSH]
• Subjects:
  Animals Cells, Cultured Environmental Monitoring Laboratories Microbiology Occupational Exposure Occupational Health Safety Vanadium Compounds
• Keywords:
  Animal-studies Cell-cultures Exposure-assessment Exposure-levels Laboratory-animals Microorganisms Occupational-exposure Vanadium-compounds
• ISSN:
  0098-4108
• Document Type:
  Text
• Funding:
  Grant
• Genre:
  Journal Article ; Journal Article
• Place as Subject:
  New York ; OSHA Region 2
• CIO:
  National Institute for Occupational Safety and Health (NIOSH) ; National Institute for Occupational Safety and Health (NIOSH)
• Topic:
  Workplace Safety & Health ; Workplace Safety & Health
• Location:
  North America ; North America
• Volume:
  51
• Issue:
  6
• NIOSHTIC Number:
  nn:20031024
• Citation:
  J Toxicol Environ Health A 1997 Aug; 51(6):591-608
• Email:
  cohenm@charlotte.med.nyu.edu
• CAS Registry Number:
  Ammonium vanadium oxide ((NH4)VO3) (CAS RN 7803-55-6) ; Vanadium (CAS RN 7440-62-2) ; Ammonium vanadium oxide ((NH4)VO3) (CAS RN 7803-55-6) ; Vanadium (CAS RN 7440-62-2)
• Federal Fiscal Year:
  1997
• Performing Organization:
  New York University, New York, New York
• Peer Reviewed:
  True
• Start Date:
  19930501
• Source Full Name:
  Journal of Toxicology and Environmental Health, Part A: Current Issues
• End Date:
  19960430
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:dad650e088f150805d28dc0613598e715500e3b7d419432a766ff07823f5106ecb366a348de708dd5db331b6cc28339daebe99d86b234fdb7b047b2fb8ca1944
• Download URL:
  https://stacks.cdc.gov/view/cdc/191419/cdc_191419_DS1.pdf
• File Type:
  [PDF - 878.27 KB ]