Coxsackievirus B3 infection alters the uptake of 2,3,7,8-tetrachlorodibenzo-p-dioxin into various tissues of the mouse.

The tissue uptake of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during infection was studied in a mouse model using the common human virus Coxsackievirus B3 (CB3), adapted here to the mouse. Male A/J-mice were infected with the CB3 virus and subsequently, on days 4 and 7 of the infection, injected with 0.5 microCi [14C]TCDD (about 65 micrograms/kg). An uninfected group was injected with [14C]TCDD and served as the control group. Spleen, thymus, heart, pancreas, liver and brain were dissected 24 h after isotope injection, and the [14C]TCDD content of the tissues was determined by standard liquid scintillation techniques. On day 7, whole body autoradiography was also performed, 4 h after the isotope injection. Our results clearly show that there is an increased TCDD uptake in the selected tissues during the CB3 infection and that this increased uptake is most pronounced on day 4 post inoculation, which corresponds to the peak of viraemia. It was found that the total tissue concentrations of TCDD were significantly increased on day 4 in the brain, pancreas, heart, spleen and liver. In the spleen, heart and brain they were still significantly increased on day 7. The considerable metabolic and immunological changes that generally are caused by infections might explain the change in accumulation of TCDD. It is possible that the increased uptake of TCDD affects the immune cells involved in repair of inflammatory tissue lesions, thereby affecting the progression of the disease.