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http://dx.doi.org/10.3347/kjp.2021.59.5.501

Naegleria fowleri Induces Jurkat T Cell Death via O-deGlcNAcylation  

Lee, Young Ah (Department of Environmental Medical Biology, Institute of Tropical Medicine, Yonsei University College of Medicine)
Kim, Kyeong Ah (Department of Environmental Medical Biology, Institute of Tropical Medicine, Yonsei University College of Medicine)
Shin, Myeong Heon (Department of Environmental Medical Biology, Institute of Tropical Medicine, Yonsei University College of Medicine)
Publication Information
Parasites, Hosts and Diseases / v.59, no.5, 2021 , pp. 501-505 More about this Journal
Abstract
The pathogenic free-living amoeba Naegleria fowleri causes primary amoebic meningoencephalitis, a fatal infection, by penetrating the nasal mucosa and migrating to the brain via the olfactory nerves. N. fowleri can induce host cell death via lytic necrosis. Similar to phosphorylation, O-linked β-N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) is involved in various cell-signaling processes, including apoptosis and proliferation, with O-GlcNAc addition and removal regulated by O-GlcNAc transferase and O-GlcNAcase (OGA), respectively. However, the detailed mechanism of host cell death induced by N. fowleri is unknown. In this study, we investigated whether N. fowleri can induce the modulation of O-GlcNAcylated proteins during cell death in Jurkat T cells. Co-incubation with live N. fowleri trophozoites increased DNA fragmentation. In addition, incubation with N. fowleri induced a dramatic reduction in O-GlcNAcylated protein levels in 30 min. Moreover, pretreatment of Jurkat T cells with the OGA inhibitor PUGNAc prevented N. fowleri-induced O-deGlcNAcylation and DNA fragmentation. These results suggest that O-deGlcNAcylation is an important signaling process that occurs during Jurkat T cell death induced by N. fowleri.
Keywords
Naegleria fowleri; O-GlcNAcylation; host cell death;
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