Cytotoxicity in feline leukemia virus subgroup-c infected fibroblasts is mediated by adherent bone marrow mononuclear cells |
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Authors: | Kanwar Nasir M Khan Gary J Kociba Maxey L Wellman Jolene A Reiter |
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Institution: | (1) Department of Veterinary Pathobiology, College of Veterinary Medicine, Ohio State University, 43210 Columbus, Ohio |
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Abstract: | Summary The pathogenesis of retrovirus-induced erythroid aplasia in cats is unknown. In studies to define mechanisms of cytotoxicity
associated with retroviral infections, bone marrow mononuclear cells (BMMC) from healthy specific pathogenfree cats were co-cultured
with uninfected feline embryonic fibroblasts (FEA cells) and FEA cells infected with feline leukemia virus (FeLV) of subgroup
A (FEA-A) or subgroup C (FEA-C). Moderate to marked cytotoxicity (CPE) developed in co-cultures of BMMC and FEA-C cells on
Days 5 to 7 of incubation but not in co-cultures of BMMC and FEA-A or BMMC and uninfected cells (FEA-CT). Cytotoxicity was
associated with adherent cells of light density (1.056) from bone marrow and peripheral blood, which were positive for alpha
naphthyl butyrate esterase activity. Stimulation of adherent cells with phorbol ester or addition of recombinant human tumor
necrosis factor-alpha (rhTNF-α) caused similar CPE in FEA-CT cells. The TNF-α concentrations in the culture supernatants of BMMC+FEA-C were higher than those of BMMC+FEA-A or BMMC+FEA-CT, and addition
of anti-TNF antibodies to the cultures blocked the CPE. These data support the hypothesis that macrophages exposed to FeLV-C
cause CPE in co-cultures of BMMC and FEA cells by a mechanism involving TNF-α. It is suggested that TNF-α may be involved in the suppression of hematopoiesis in cats which develop FeLV-C induced erythroid aplasia. |
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Keywords: | cytotoxicity retrovirus feline leukemia virus TNF-α |
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