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Real-Time Quantification of Reactive Oxygen Species in Neutrophils Infected with Meningitic Escherichia Coli
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Real-Time Quantification of Reactive Oxygen Species in Neutrophils Infected with Meningitic Escherichia Coli

Published on: April 20, 2021

A role for reactive oxygen species in endotoxin-induced elevation of MOR expression in the nervous and immune systems

Erik F Langsdorf1, Xin Mao, Sulie L Chang

  • 1Institute of NeuroImmune Pharmacology, Seton Hall University, 400 South Orange Ave., South Orange, NJ 07079, USA.

Journal of Neuroimmunology
|June 21, 2011
PubMed

Insights

Lipopolysaccharide (LPS) exposure increases mu-opioid receptor (MOR) expression in immune cells via reactive oxygen species (ROS). This effect extends to neuronal cells, highlighting neuroimmune axis crosstalk.

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • The neuroimmune axis describes the bidirectional communication between the nervous and immune systems.
  • Mu-opioid receptors (MOR) are crucial in pain modulation and immune responses.
  • Lipopolysaccharide (LPS) is a potent immune activator with known systemic effects.

Purpose of the Study:

  • To elucidate the mechanism by which LPS influences MOR expression in immune and neuronal cells.
  • To investigate the role of reactive oxygen species (ROS) in LPS-induced MOR modulation.
  • To explore the communication pathways between immune cells and neurons in response to LPS.

Main Methods:

  • Utilized an in vitro conditioned medium model system.
  • Exposed macrophage-like TPA-HL-60 cells to LPS and measured ROS and MOR expression.
  • Applied conditioned medium from LPS-stimulated cells to neuronal SH-SY5Y cells to assess MOR expression changes.
  • Investigated the involvement of TNF-α and GM-CSF in the observed effects.

Main Results:

  • LPS exposure stimulated intracellular ROS accumulation and increased MOR expression in TPA-HL-60 cells.
  • Conditioned medium from LPS-treated TPA-HL-60 cells elevated MOR expression in SH-SY5Y neuronal cells.
  • The increase in neuronal MOR expression was mediated by tumor necrosis factor-alpha (TNF-α) and granulocyte-macrophage colony-stimulating factor (GM-CSF).

Conclusions:

  • LPS modulates MOR expression in both immune and neuronal cells through ROS signaling.
  • Demonstrates significant crosstalk within the neuroimmune axis, influenced by endotoxin exposure.
  • Suggests potential therapeutic targets for conditions involving neuroinflammation and opioid signaling.

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