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Immunohistochemical localization of galectin-3 in the brain with Theiler's murine encephalomyelitis virus (DA strain) infection
2013
Shin, T., Jeju National University, Jeju, Republic of Korea | Carrillo-Salinas, F.J., Instituto Cajal, CSIC, Madrid, Spain | Mart'nez, A.F., Instituto Cajal, CSIC, Madrid, Spain | Mecha, M., Instituto Cajal, CSIC, Madrid, Spain | Guaz,a C., Instituto Cajal, CSIC, Madrid, Spain
Galectin-3 is a β-galactoside-binding lectin that plays a role in neuroinflammation through cell migration, proliferation, and apoptosis. In the present study, regulation of galectin-3 was examined in the brain of mice infected with the Daniel strain of Theiler’s murine encephalomyelitis virus (TMEV) at days 7 and 81 post-infection by immunohistochemistry. Immunohistochemistry revealed that galectin-3 was mainly localized in ionized calcium-binding adapter 1-positive macrophages/activated microglia, but not in Iba-1-positive ramified microglia. Galectin-3 was also weakly detected in some astrocytes in the same encephalitic lesions, but not in neurons and oligodendrocytes. Collectively, the present findings suggest that galectin-3, mainly produced by activated microglia/macrophages, may be involved in the pathogenesis of virus induced acute inflammation in the early stage as well as the chronic demyelinating lesions in Daniel strain of TMEV induced demyelination model.
Afficher plus [+] Moins [-]Alternatively activated M2 macrophages increase in early stages of experimental autoimmune myocarditis in Lewis rats
2013
Oh, H., Jeju National University, Jeju, Republic of Korea | Ahn, M., Jeju National University, Jeju, Republic of Korea | Matsumoto, Y., Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan | Shin, T., Jeju National University, Jeju, Republic of Korea
To better understand the role of macrophages in early stages of experimental autoimmune myocarditis (EAM), we compared the expression of inducible nitric oxide synthase (iNOS) and arginase-1, markers for classically activated M1 and alternatively activated M2 macrophages, respectively, in the hearts of EAM-affected and control rats. Immunohistochemical evidence revealed that both iNOS-positive and arginase 1-positive macrophages were found in EAM lesions, while some cells were co-localized with both markers. This finding suggests that the increased level of arginase-1, which is partly from M2 macrophages, contributes to the modulation of EAM, possibly through the reduction of nitric oxide in the lesion.
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