Early microlesion of viral encephalitis confirmed by galectin-3 expression after a virus inoculation

Kazuhiro Kobayashi, Masayuki Niwa, Masato Hoshi, Kuniaki Saito, Kenji Hisamatsu, Yuichiro Hatano, Hiroyuki Tomita, Tatsuhiko Miyazaki, Akira Hara

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)107-112
Number of pages6
JournalNeuroscience Letters
Volume592
DOIs
Publication statusPublished - 01-04-2015

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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