The
flame retardant component 2,2',4,4',5-penta-BDE (BDE-99) is found in the environment and in human tissues and fluids. In mice the common human coxsackievirus B3 (CVB3)
infection has been shown to change the tissue distribution of
BDE-99. We now investigate how CVB3
infection in mice affects liver uptake of (14)C at two doses of radiolabelled
BDE-99, and whether increased tissue levels are related to changed virus replication and gene expression of the proinflammatory
chemokine monocyte chemoattractant protein-1 (MCP-1). Mice were infected on day 0, orally treated either with 200μg or 20mg (14)C-BDE-99/kgbw on day 1, and euthanised on day 3. Serum and liver levels of (14)C-BDE-99, as well as virus levels and gene expressions of MCP-1 in the liver, were measured. In non-infected mice, there was a dose-dependent uptake of
BDE-99 in both liver and serum, and in infected animals the liver
BDE-99 levels was further increased. When comparing infected mice exposed to the two
BDE-99 doses, the higher BDE dose resulted in increased virus amounts in the liver, and decreased
infection-induced expression of MCP-1. Consequently, a high enough dose/tissue concentration of
BDE-99 may result in a disturbed mobilisation of immune cells into infected tissues that could explain higher virus titres and a possibly altered
clinical course of the disease. Moreover, the fact that CVB3
infection increased the
BDE-99 levels in liver but not in serum may impair the risk assessment of
polybrominated diphenyl ethers (
PBDEs) in subclinical and clinically infected individuals, as serum levels is the common marker of exposure.