The magnitude of inflammatory lesions in the hearts of coxsackie B3 (C
B3)-virus infected mice can be affected by the potentially toxic heavy
metals cadmium (Cd), nickel (Ni) and methyl mercury (MeHg). The infec
tion is associated with a changed distribution, such as Cd accumulatio
n in the spleen and kidneys. New target organs for Ni during the infec
tion were the heart, pancreas and lungs in which inflammatory lesions
were present. This increased uptake was correlated with the disturbed
function of immune cells and an increased inflammatory reaction. Ni an
d MeHg appeared to have a direct effect on immune cells that resulted
in changed natural killer cell activity and decreased mobilization of
macrophages, CD4(+) and CD8(+) cells into the inflammatory lesions. Al
though MeHg increased spleen T cell activity and gamma-interferon (IFN
-gamma) levels, the inflammatory lesions in the heart increased Anothe
r detrimental effect of MeHg treatment was evident by an increased cal
cium and decreased zinc content in the inflamed heart, which may partl
y explain the more severe inflammatory lesion. The host's response, CB
3 infection, changed the distribution of each metal in a specific way,
a fact which may subsequently result in altered target organ toxicity
and resistance to the infection.