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<p>Chronic inflammation, resulting from infections, is characterized by increased levels of cytokines including interleukin-1 (IL-1), but little is known about how IL-1 contributes to cognitive impairment, potentially via epigenetic processes. Here we demonstrate that mice chronically infected with the parasite <i>Toxoplasma gondii</i> exhibit impaired spatial memory, which is dependent on neuronal IL-1 signaling and mimicked by chronic exposure to IL-1β. Both <i>T. gondii</i> infection and chronic IL-1β drive H2A.X-dependent DNA double-strand break signaling in hippocampal neurons and invalidating neuronal H2A.X-dependent signaling blocks memory impairments caused by either exposure. Our results highlight the instrumental role of cytokine-induced double-strand-break-dependent signaling in spatial memory defects, which may be relevant to multiple brain diseases.</p>

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Toxoplasma gondii infection and chronic IL-1 elevation drive hippocampal DNA double-strand break signaling, leading to cognitive deficits

  • 期刊论文

  • 发表日期：

    2025年8月21日

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  • Marcy Belloy,
  • Benjamin A. M. Schmitt,
  • Florent H. Marty,
  • Charlotte Paut,
  • Emilie Bassot,
  • Amel Aïda,
  • Marine Alis,
  • Margot Zahm,
  • Adeline Chaubet,
  • Hugo Garnier,
  • Thelma Flores-Aguilar,
  • Elisa Roitg,
  • Renzo Gutierrez-Loli,
  • Sophie Allart,
  • Romain Ecalard,
  • Raphaël Boursereau,
  • Gaëtan Ligat,
  • Daniel Gonzalez-Dunia,
  • Nicolas Blanchard,
  • Elsa Suberbielle

摘要

Chronic inflammation, resulting from infections, is characterized by increased levels of cytokines including interleukin-1 (IL-1), but little is known about how IL-1 contributes to cognitive impairment, potentially via epigenetic processes. Here we demonstrate that mice chronically infected with the parasite Toxoplasma gondii exhibit impaired spatial memory, which is dependent on neuronal IL-1 signaling and mimicked by chronic exposure to IL-1β. Both T. gondii infection and chronic IL-1β drive H2A.X-dependent DNA double-strand break signaling in hippocampal neurons and invalidating neuronal H2A.X-dependent signaling blocks memory impairments caused by either exposure. Our results highlight the instrumental role of cytokine-induced double-strand-break-dependent signaling in spatial memory defects, which may be relevant to multiple brain diseases.