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IL-10/β-Endorphin-Mediated Neuroimmune Modulation on Microglia during Antinociception
Thiago Caetano Andrade Belo1, Gabriela Xavier Santos2, Bruno Eduardo Gabriel da Silva2
1Laboratory of Molecular Biology of Microorganisms, Federal University of Alfenas, Alfenas 37130-001, Brazil.
Brain Sciences
|May 27, 2023
Summary
Interleukin-10 (IL-10) and beta-endorphin pathways reduce pain by modulating microglia activity. This review highlights how IL-10 stimulates pathways that increase beta-endorphin, inhibiting pain signals.
Area of Science:
- Neuroimmunology
- Pain Research
- Molecular Biology
Background:
- Microglia play a key role in pain pathophysiology via neuroimmune regulation.
- Interleukin-10 (IL-10) is an anti-inflammatory cytokine that influences pain perception.
- Beta-endorphin is an endogenous opioid peptide involved in analgesia.
Purpose of the Study:
- To review recent advances in understanding the mechanism of IL-10/beta-endorphin in pain reduction.
- To summarize how IL-10/beta-endorphin signaling alleviates nociceptive stimuli.
Main Methods:
- Systematic literature search of databases up to November 2022.
- Data extraction and methodological quality assessment by two independent reviewers.
- Inclusion of seventeen eligible studies for the review.
Main Results:
- IL-10 stimulates receptors (GLP-1R, GRP40, α7nAChR) and signaling pathways (STAT3) to enhance beta-endorphin expression and secretion.
- Various molecules (gabapentinoids, thalidomide, etc.) and electroacupuncture reduce pain via IL-10-mediated, microglia-dependent beta-endorphin increase.
- Beta-endorphin binding to µ-opioid receptors inhibits nociceptive stimuli through neuronal hyperpolarization.
Conclusions:
- The IL-10/beta-endorphin pathway is a critical mechanism for pain reduction.
- This pathway involves microglia-neuron crosstalk and is influenced by diverse pharmacological and non-pharmacological interventions.
- Understanding this neuroimmunological axis offers insights into novel pain management strategies.
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