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Interleukin-27 controls basal pain threshold in physiological and pathological conditions
Tomoko Sasaguri1, Toru Taguchi2,3, Yuzo Murata4
1Department of Anesthesiology & Critical Care Medicine, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga, 849-8501, Japan.
Scientific Reports
|July 25, 2018
Summary
Interleukin-27 (IL-27) constitutively controls pain sensation thresholds. Its absence causes chronic pain hypersensitivity, suggesting a novel pain regulatory mechanism.
Area of Science:
- Neuroimmunology
- Pain Research
- Cytokine Signaling
Background:
- Pain sensation is modulated by immune molecules like cytokines.
- Interleukin-17 (IL-17) promotes pain, while Interleukin-10 (IL-10) suppresses it.
- IL-27 exhibits anti-inflammatory effects by modulating T cell differentiation, reducing IL-17 and increasing IL-10.
Purpose of the Study:
- To investigate the regulatory role of Interleukin-27 (IL-27) in pain sensation.
- To determine if IL-27 controls thermal and mechanical sensory thresholds.
Main Methods:
- Utilized knockout mouse models lacking IL-27 or its receptor WSX-1.
- Administered IL-27 to IL-27-deficient mice to assess reversal of hypersensitivity.
- Evaluated hypersensitivity in inflammatory and neuropathic pain models in IL-27/WSX-1 deficient mice.
Main Results:
- Mice lacking IL-27 or WSX-1 exhibited spontaneous chronic pain-like hypersensitivity to thermal and mechanical stimuli.
- Reconstitution of IL-27 reversed these hypersensitive behaviors.
- Absence of IL-27/WSX-1 signaling exacerbated hypersensitivity in established pain models.
Conclusions:
- Endogenous IL-27 constitutively regulates pain sensation thresholds under physiological and pathological conditions.
- IL-27 functions as a key mediator in pain control, distinct from typical inflammatory cytokines.
- Disruption of IL-27/WSX-1 signaling reveals a novel mechanism contributing to chronic pain hypersensitivity.
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