title: Changed distribution and immune effects of nickel augment viral-induced inflammatory heart lesions in mice.
abstract: We have used the myocarditic coxsackievirus B3 (CB3) infection in Balb/c mice to investigate immunotoxic effects of a ten-week low-dose (0.002 M) administration of nickel chloride (NiCl2) prior to infection. This dose did not influence CB3-induced mortality. Whole-body autoradiography of [63Ni] during the disease showed the pancreas, lungs and myocardium to be new target organs in this disease. Seven days after the inoculation, impulse counting of these organs showed the infection-induced increase of [63Ni] 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. Nickel tended to increase spleen B- and T-cell activities, but thymocyte activity was unaffected. The activity of spleen natural killer (NK) cells decreased by 30% (P < 0.05), whereas blood-cell activity in fact increased by 51% (P < 0.05). The inflammatory and necrotic lesions in the 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-treated mice. The response pattern of lymphocyte subsets in situ in myocardial inflammatory lesions was elucidated by an immune histochemical staining 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 correlated to the size of the inflammatory area (r = -0.529, P < 0.02). The results 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.
authors.affiliation: Kabi Pharmacia AB, Helsingborg, Sweden.
authors.forename: N G
authors.initials: NG
authors.lastname: Ilbäck
authors.forename: J
authors.initials: J
authors.lastname: Fohlman
authors.forename: G
authors.initials: G
authors.lastname: Friman
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001345:Autoradiography; D003384:Coxsackievirus Infections / Q000276:immunology*; D029822:Enterovirus B, Human / Q000276:immunology*; D005260:Female; D007111:Immunity, Cellular / Q000187:drug effects; D007275:Injections, Intravenous; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000276:immunology* / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D009532:Nickel / Q000276:immunology / Q000493:pharmacokinetics / Q000633:toxicity*; D011897:Random Allocation; D013154:Spleen / Q000187:drug effects / Q000276:immunology; D013950:Thymus Gland / Q000187:drug effects / Q000276:immunology; D014018:Tissue Distribution
chemical_list: C022838:nickel chloride; D009532:Nickel