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Research Article

Oral tungstate (Na2WO4) exposure reduces adaptive immune responses in mice after challenge

, , , , , & show all
Pages 148-159 | Received 26 Apr 2013, Accepted 12 Jun 2013, Published online: 29 Jul 2013
 

Abstract

Tungstate has been identified as a ground water contaminant at military firing ranges and can be absorbed by ingestion. In this study, C57BL6 mice were exposed to sodium tungstate (Na2WO4·2H2O) (0, 2, 62.5, 125, and 200 mg/kg/day) in their drinking water for an initial 28-day screen and in a one-generation (one-gen) model. Twenty-four hours prior to euthanasia, mice were intraperitoneally injected with Staphylococcal enterotoxin B (SEB) (20 μg/mouse) or saline as controls. After euthanasia, splenocytes and blood were collected and stained with lymphocyte and/or myeloid immunophenotyping panels and analyzed by flow cytometry. In the 28-day and one-gen exposure, statistically significant reductions were observed in the quantities of activated cytotoxic T-cells (TCTL; CD3+CD8+CD71+) and helper T-cells (TH; CD3+CD4+CD71+) from spleens of SEB-treated mice. In the 28-day exposures, CD71+ TCTL cells were 12.87 ± 2.05% (SE) in the 0 tungstate (control) group compared to 4.44 ± 1.42% in the 200 mg/kg/day (p < 0.001) group. TH cells were 4.85 ± 1.23% in controls and 2.76 ± 0.51% in the 200 mg/kg/day (p < 0.003) group. In the one-gen exposures, TCTL cells were 7.98 ± 0.49% and 6.33 ± 0.49% for P and F1 mice after 0 mg/kg/day tungstate vs 1.58 ± 0.23% and 2.52 ± 0.25% after 200 mg/kg/day of tungstate (p < 0.001). Similarly, TH cells were reduced to 6.21 ± 0.39% and 7.20 ± 0.76%, respectively, for the 0 mg/kg/day P and F1 mice, and 2.28 ± 0.41% and 2.85 ± 0.53%, respectively, for the 200 mg/kg/day tungstate P and F1 groups (p < 0.001). In delayed-type hypersensitivity Type IV experiments, tungstate exposure prior to primary and secondary antigen challenge significantly reduced footpad swelling at 20 and 200 mg/kg/day. These data indicate that exposure to tungstate can result in immune suppression that may, in turn, reduce host defense against pathogens.

Acknowledgements

We would like to thank our summer interns, Connie Fu, Thomas Park, Michael Sun, and Elizabeth Marconne, for their help in the day-to-day management of this study. We would also like to thank staff of the Environmental Health Effects Laboratory at Wright-Patterson Air Force Base. These individuals helped in various ways during the experiments: Sue Prues, Tracy Doyle, Shawn McInturf, Pedro Ortiz, Karen Mumy, and Michelle Okolica.

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