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



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  • Personal Author:
  • 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:
  • Keywords:
  • ISSN:
    0098-4108
  • Document Type:
  • Funding:
  • Genre:
  • Place as Subject:
  • CIO:
  • Topic:
  • Location:
  • 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:
  • 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):
  • Main Document Checksum:
    urn:sha-512:dad650e088f150805d28dc0613598e715500e3b7d419432a766ff07823f5106ecb366a348de708dd5db331b6cc28339daebe99d86b234fdb7b047b2fb8ca1944
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  • File Type:
    Filetype[PDF - 878.27 KB ]
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