Common
viral infections have been shown to change the tissue distribution of
xenobiotics, including
polybrominated diphenyl ethers (
PBDEs). In previous studies, it has been shown that CYP2B gene expression is induced after
PBDE exposure whereas coxsackievirus B3 (CBV3)
infection suppresses the expression of CYP-gene expression in the liver. In the present study, CVB3 adapted to Balb/c mice was used to study the combined effects of
infection and exposure to pure
BDE-99 or the commercial mixture Bromkal on
CYP1A1 and CYP2B expression in the lungs and pancreas on day 3 of the
infection. The quantitative gene expression of virus,
CYP1A1 and CYP2B was measured by real-time polymerase chain reaction (RT-PCR).
PBDE exposure in the non-infected mice tended to increase CYP2B expression in the lungs but not in the pancreas.
Infection in both non-exposed and
PBDE-exposed mice increased CYP2B expression in the lungs but was non-detectable in the pancreas. In the non-infected mice
PBDE exposure left the
CYP1A1 expression unaltered in both the lungs and pancreas.
Infection in both non-exposed and
PBDE-exposed mice tended to decrease the gene expression of
CYP1A1 in the lungs but to induce it in the pancreas. A correlation between the amount of virus and the gene expression of CYP2B was found in the lungs. However, no effects of
PBDE on virus replication were observed in any organ. In conclusion,
viral infection affects CYP-gene expression differently in the pancreas and lungs whereas
PBDE-induced effects were not obvious. The organ-specific change in gene expression could explain a changed tissue distribution of
xenobiotics during
infection.