Immunological studies on mechanism for teeth hypoplasia following virus infection in mouse model

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The purpose of this study was to examine the mechanisms that teeth hypodisplasia of mice were caused following virus infection. The relationship between teeth hypoplasia and systematic inflammation was addressed.Newborn mice were inculated intraperitoneally (IP) with mouse cytomegalovirus (MCMV) smith strain. Mice were killed and their incisor teeth were observed with SEM. The findings showed that the surface of incisors were rough in the site formed in the acute phase of virus infection. Then, the cytokine expression was examined by using cytokine microarray. The results showed that IL-2, IL-4, IL-5, 11-6, IL-10, IL-17, MCP-1, TPO and VEGF changed after virus infection. Nest, kinetics of histidine decarboxylase (HDC) activities, as index of inflammation of tissues, and cytokine were studied. Four- weeks of age mice were inoculated IP with MCMV. On 1 to 13th days after the infection, various organs were sampled, and their HDC activities and the level of cytokines were analyzed. MCMV were isolated in spleen and liver when those HDC activity elevated. The time course that HDC activities elevate were different among organs. The data of cytokine kinetics showed that the levels of VEGF and TNF-α decreased significantly in spleen. In liver, the levels of IL-12, TNF-α, IL-6 increased significantly. In lung, IL-1 increased and IL-6 decreased. IFN-γ level increased on 13th after MCMV infection.These data suggested that host's inflammation response was big after virus infection, and continued over 10 days in various organs. Altered level of chemokines may influence the migration and activation of leukocytes to the site of virus infection. Histamine, produced by the result from enhancement of HDC activity, causes changes of micro-circulation system, enhances vascular permeability. In conclusion, as vascular system play a role in the teeth forming period, the systematic inflammation following virus infection affect teeth formation.