Abstract
BackgroundAdministration of mercury at nontoxic doses induces systemic autoimmune disease in Brown Norway (BN) rats. The pathogenesis of lupus-like oral mucosal lesion by mercury-induced autoimmunity is still unclear, even though the oral mucosa is observed to be commonly affected in mercury-treated BN rats. In this study, we investigated the immunopathology of lupus-like oral mucosal lesions in a model of mercury-induced systemic autoimmunity.MethodsBrown Norway male rats were injected subcutaneously with either phosphate-buffered saline (control) or mercury at a dose of 1.0 mg per kilogram of body weight on days 0, 3, 5, and 7. Blood, kidney, and tongue samples were taken at various timepoints for evaluation by immunohistochemistry, RT-PCR, and lupus band test (LBT).ResultsOral mucosal lesions were classified according to three consecutive temporal phases on the basis of infiltration of immunocompetent cells as follows: (phase I) infiltration of MHC class II+ dendritic cells (DC) and macrophages; (phase II) addition of ED1+ macrophage infiltrates; and (phase III) focal infiltration of pan T cells following increased infiltration of DC and macrophages. Dense infiltration of DC and macrophages was observed in the basement membrane (BM) zone of the oral epithelium. Tissue expression of IL-4 mRNA was detected in early lesions (phase I), suggesting that locally produced IL-4 may be responsible for Th2-mediated immune response. A linear and continuous smooth pattern of fluorescence was observed in the oral epithelial BM in addition to renal glomeruli, indicating immune complex deposits.ConclusionsLocal autoimmune responses are involved in the pathogenesis of mercury-induced lupus-like lesions of the oral mucosa.
Highlights
Administration of mercury at nontoxic doses induces systemic autoimmune disease in Brown Norway (BN) rats
Local autoimmune responses are involved in the pathogenesis of mercury-induced lupus-like lesions of the oral mucosa
Immunohistochemical staging of mercury-induced oral mucosal lesions by mononuclear cell infiltrates We first analyzed infiltration of the oral mucosa from the control and mercury-treated rats by MHC class II+, ED1+, and CD5+ cells and classified the oral mucosal lesions according to three consecutive phases on the basis of density and distribution of infiltrating cells (Figures 1, 2 and 3)
Summary
Administration of mercury at nontoxic doses induces systemic autoimmune disease in Brown Norway (BN) rats. The pathogenesis of lupus-like oral mucosal lesion by mercury-induced autoimmunity is still unclear, even though the oral mucosa is observed to be commonly affected in mercury-treated BN rats. We investigated the immunopathology of lupus-like oral mucosal lesions in a model of mercury-induced systemic autoimmunity. Induction of autoimmune disease by environmental agents, especially mercury, in susceptible rodent strains is These changes seem to result from the establishment of mercury-induced autoimmunity in the oral mucosa. Some authors suggest that oral lesions are present in 9% - 45% patient with systemic LE and 3% -20% in those with cutaneous LE [11] These clinical data prompted us to examine whether systemic autoimmunity can lead to established lupus lesions in the oral mucosa. We examined oral mucosal lesions in BN rats with systemic mercury-induced autoimmunity. Our data demonstrate that systemic mercury-induced autoimmunity induces LE-like lesions in the oral mucosa
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