CHANGED DISTRIBUTION AND IMMUNE EFFECTS OF NICKEL AUGMENT VIRAL-INDUCED INFLAMMATORY HEART LESIONS IN MICE

We have used the myocarditic coxsackievirus B3 (CB3) infection in Balb /c mice to investigate immunotoxic effects of a ten-week low-dose(0.00 2 M) administration of nickel chloride (NiCl2) prior to infection. Thi s dose did not influence CB3-induced mortality. Whole-body autoradiogr aphy of [Ni-63] during the disease showed the pancreas, lungs and myoc ardium to be new target organs in this disease. Seven days after the i noculation, impulse counting of these organs showed the infection-indu ced increase of [Ni-63] to be, 5-fold (P < 0.01) in the pancreas, 2.2- fold (P < 0.05) in the lungs and 1.3-fold (P < 0.05) in the heart. Nic kel tended to increase spleen B- and T-cell activities, but thymocyte activity was unaffected. The activity of spleen natural killer (NK) ce lls decreased by 30% (P < 0.05), whereas blood-cell activity in fact i ncreased by 51%(P < 0.05). The inflammatory and necrotic lesions in th e ventricular myocardium seven days after the inoculation covered 3.31 % of the tissue section area in infected control mice. This damage was increased by 43% (to 4.74% of the tissue section area) in nickel-trea ted mice. The response pattern of lymphocyte subsets in situ in myocar dial inflammatory lesions was elucidated by an immune histochemical st aining technique. The number of cytotoxic T-cells, helper T-cells and Mac 2(+) cells (macrophages) in these lesions decreased by 46% (P < 0. 05), 41% (P < 0.05) and 27% (not significant), respectively, with the nickel treatment. The number of helper T-cells was negatively correlat ed to the size of the inflammatory area (r = -0.529, P < 0.02). The re sults indicate that nickel may contribute to the progression of target organ pathology in infection-induced diseases of an autoimmune and/or inflammatory character, such as diabetes and myocarditis.