Decreased resistance to Listeria monocytogenes in mice following vanadate exposure: effects upon the function of macrophages.

We have previously demonstrated that ammonium metavanadate has a broad immunomodulating effect in mice after subchronic exposure. Because host resistance to pathogenic Listeria monocytogenes and in vitro phagocytic activity of harvested peritoneal macrophages (PEM) were strongly affected by vanadate treatment, we investigated the effect of vanadate on the functional role of resident PEM in active listeriosis in the mouse. Vanadium treatment results in altered patterns of clearance of the organism from the peritoneal cavity, liver and spleen. The total in vitro phagocytic uptake of Listeria by PEM was consistently decreased as a function of infection period. Similarly, intracellular killing of Listeria was decreased although the PEM from the vanadate-treated and control mice were more bacteriostatic than bactericidal. Population distributions of Listeria within infected PEM were not affected by host pretreatment with vanadate. Vanadate exposure interferes with both the uptake and ultimate intraphagolysosomal killing of Listeria. These results were expected in light of our previous studies of the effects of vanadate on PEM superoxide production, and hexose monophosphate shunt and glutathione redox cycle activity. The results provide additional information for the development of a mechanism to explain why workers exposed to vanadium-containing dusts have increased susceptibility to bacterial respiratory diseases.