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M1-Type Microglia-Derived Extracellular Vesicles Overexpressing IL-1R1 Promote Postoperative Cognitive Dysfunction by

Zheng Qi1,2, Yang Yu1,2, Yu Su3

  • 1Department of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe Dong Road, Zhengzhou, 450000, People's Republic of China.

Inflammation
|July 28, 2023
PubMed

Insights

Extracellular vesicles from activated M1-type microglia worsen postoperative cognitive dysfunction (POCD) by promoting neuronal inflammation and memory deficits. These EVs contribute to synaptic loss and neuron degeneration, highlighting a novel mechanism in POCD development.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Postoperative cognitive dysfunction (POCD) is a common complication following surgery and anesthesia, characterized by memory impairment and cognitive decline.
  • Activated microglia, particularly M1-type, release inflammatory factors that can lead to neuronal damage via pathways like NF-κB signaling.
  • The precise mechanisms underlying POCD pathogenesis remain incompletely understood, necessitating further investigation into cellular and molecular contributors.

Purpose of the Study:

  • To investigate the role of extracellular vesicles derived from M1-type microglia (EVsM1-Microglia) in the pathological processes of POCD.
  • To elucidate the impact of EVsM1-Microglia on synaptic integrity, neuronal degeneration, and cognitive function in a surgical mouse model.

Main Methods:

  • Surgical procedures were performed on mice to induce POCD.
  • Levels of NF-κB phosphorylation, IL-1β, PSD95, and MAP2 were measured in hippocampal neurons.
  • Microglia activation, synaptic structures, and the effects of EVsM1-Microglia (with and without IL-1R1 siRNA) on neuronal health and memory were assessed.

Main Results:

  • Surgery significantly increased NF-κB phosphorylation and IL-1β, while decreasing PSD95 and MAP2 in hippocampal neurons, indicating neuronal damage and inflammation.
  • Surgery induced microglia activation, reduced synaptic density, and caused neuronal degeneration, effects partially mitigated by IL-1R1 siRNA.
  • EVsM1-Microglia exacerbated synaptic loss, neuron degeneration, and memory deficits in surgical mice, independent of surgery or microglia activation itself.

Conclusions:

  • M1-type microglia-derived extracellular vesicles (EVsM1-Microglia) play a significant role in promoting POCD development.
  • EVsM1-Microglia, particularly those with high IL-1R1 expression, contribute to POCD by inducing neuronal inflammation, synaptic loss, and cognitive impairment.
  • Targeting EVsM1-Microglia or their inflammatory signaling pathways presents a potential therapeutic strategy for mitigating POCD.
Keywords:
anesthesiaextracellular vesiclespostoperative cognitive dysfunctionsurgery

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