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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)
  • 투고 : 2021.07.30
  • 심사 : 2021.09.17
  • 발행 : 2021.10.31

초록

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.

키워드

과제정보

This research was supported by a faculty research grant from Yonsei University College of Medicine (6-2015-0063).

참고문헌

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