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Pain control in inflammation governed by selectins
H Machelska1, P J Cabot, S A Mousa
1Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, MD 21287-8711, USA.
Nature Medicine
|December 10, 1998
Summary
Immune cells release beta-endorphin to reduce pain at inflamed sites. Blocking immune cell (immunocyte) migration to these sites inhibits this natural pain relief, highlighting a link between immunity and pain control.
Area of Science:
- Neuroimmunology
- Pain Research
- Cellular Biology
Background:
- Opioid-containing immune cells migrate to inflamed tissues, releasing beta-endorphin to activate peripheral opioid receptors and inhibit pain.
- Immunocyte recruitment involves sequential adhesion molecule engagement between immune cells and vascular endothelium.
- Selectins play a crucial role in the initial extravasation of immunocytes into inflamed areas.
Purpose of the Study:
- To investigate the role of selectins in endogenous and corticotropin-releasing factor-induced peripheral opioid analgesia.
- To determine if blocking immunocyte infiltration affects beta-endorphin-mediated pain relief.
Main Methods:
- Utilized anti-selectin treatment to block immunocyte migration.
- Assessed the impact of this blockade on peripheral opioid analgesia.
- Measured beta-endorphin levels in inflamed tissues following treatment.
Main Results:
- Anti-selectin treatment abolished peripheral opioid analgesia induced by stress or corticotropin-releasing factor.
- This blockade prevented the infiltration of beta-endorphin-containing immunocytes into inflamed tissues.
- Consequently, beta-endorphin levels in the inflamed tissue were reduced.
Conclusions:
- The immune system utilizes cell migration mechanisms for pain control in injured tissues, not solely for pathogen defense.
- Inhibiting the immigration of opioid-producing cells exacerbates pain.
- Analgesia can be achieved by promoting adhesive interactions that recruit opioid-producing immunocytes to injured sites.
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