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Naegleria fowleri Induces Jurkat T Cell Death via O-deGlcNAcylation

Young Ah Lee1, Kyeong Ah Kim1, Myeong Heon Shin1

  • 1Department of Environmental Medical Biology, Institute of Tropical Medicine, Yonsei University College of Medicine, Seoul 03722, Korea.

The Korean Journal of Parasitology
|November 2, 2021
PubMed

Insights

Naegleria fowleri infection triggers O-linked β-N-acetylglucosamine (O-GlcNAc) removal, leading to DNA fragmentation and cell death in Jurkat T cells. Inhibiting O-GlcNAc removal prevents this cell death.

Area of Science:

  • Cell Biology
  • Infectious Diseases
  • Molecular Biology

Background:

  • Naegleria fowleri causes fatal primary amoebic meningoencephalitis by invading the brain.
  • O-linked β-N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) regulates cell signaling, including apoptosis.
  • The precise mechanism of N. fowleri-induced host cell death remains unclear.

Purpose of the Study:

  • To investigate if N. fowleri modulates O-GlcNAcylated proteins during cell death in Jurkat T cells.
  • To explore the role of O-GlcNAcylation in N. fowleri-induced host cell death.

Main Methods:

  • Jurkat T cells were co-incubated with live N. fowleri trophozoites.
  • O-GlcNAcylated protein levels and DNA fragmentation were assessed.
  • Cells were pretreated with an O-GlcNAcase (OGA) inhibitor (PUGNAc) before N. fowleri exposure.

Main Results:

  • N. fowleri co-incubation increased DNA fragmentation in Jurkat T cells.
  • N. fowleri rapidly reduced O-GlcNAcylated protein levels within 30 minutes.
  • PUGNAc pretreatment inhibited N. fowleri-induced O-deGlcNAcylation and DNA fragmentation.

Conclusions:

  • N. fowleri infection induces O-deGlcNAcylation in Jurkat T cells.
  • O-deGlcNAcylation is a critical signaling pathway in N. fowleri-induced T cell death.
  • Targeting O-GlcNAcylation may offer therapeutic strategies against N. fowleri infections.
Keywords:
Naegleria fowleriO-GlcNAcylationhost cell death

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