Early microlesion of viral encephalitis confirmed by galectin-3 expression after a virus inoculation.
Galectin-3 is a β-galactosidase-binding lectin which is important in cell proliferation and apoptotic regulation. Encephalomyocarditis virus (EMCV), which includes the Enterovirus genus, can cause not only acute myocarditis but also neuronal degeneration of central nervous system in various animals including mice. The pathophysiological role of galectin-3 in central nervous system following acute viral infection is not fully understood. The goal of this study is to determine the localization and time-course of galectin-3 expression after acute viral inoculation with EMCV. Galectin-3 is up-regulated in degenerated lesions of brain area including cerebellum, hippocampus, thalamus and cerebral hemisphere, 96 h after EMCV inoculation. At the same time, Iba-1 positive microglia was morphologically activated within and around the focus of infection. Interestingly, in cerebellum, the microlesions containing a few galectin-3 cells were detected in the immediate-early phase of infection, as early as 48 h after EMCV inoculation. Thus, our results indicate that galectin-3 expression may be a key mediator between viral infection and neuronal degeneration in central nervous system including cerebellum. Furthermore, detection of galectin-3 might be an early diagnostic method for neuronal degeneration after virus infection.
Department of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu, Japan; Division of Pathology, Gifu University Hospital, Gifu, Japan.
Kazuhiro
K
Kobayashi
Medical Science Division, United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, Gifu, Japan. Electronic address: mniwa@gifu-u.ac.jp.
Masayuki
M
Niwa
Faculty of Medical Science, Suzuka University of Medical Science, Mie, Japan.
Masato
M
Hoshi
Human Health Sciences, Kyoto University Graduate School of Medicine and Faculty of Medicine, Kyoto, Japan.
Kuniaki
K
Saito
Department of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu, Japan.
Kenji
K
Hisamatsu
Department of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu, Japan.
Yuichiro
Y
Hatano
Department of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu, Japan.
Hiroyuki
H
Tomita
Division of Pathology, Gifu University Hospital, Gifu, Japan.
Tatsuhiko
T
Miyazaki
Department of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu, Japan.
Akira
A
Hara
D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D018188:Cardiovirus Infections / Q000378:metabolism* / Q000473:pathology; D002531:Cerebellum / Q000378:metabolism / Q000473:pathology; D018792:Encephalitis, Viral / Q000378:metabolism* / Q000473:pathology; D004686:Encephalomyocarditis virus; D037502:Galectin 3 / Q000378:metabolism*; D008297:Male; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000378:metabolism; D013997:Time Factors; D015854:Up-Regulation
D037502:Galectin 3
Cerebellum; EMCV; Galectin-3; Microglia; Neuronal degeneration