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Morphine induces splenocyte trafficking into the CNS.

Michael Olin1, Seunguk Oh, Sabita Roy

  • 1Department of Pediatrics, University of Minnesota, Minneapolis, MN 55455, USA. olin0012@umn.edu

Journal of Neuroimmune Pharmacology : the Official Journal of the Society on Neuroimmune Pharmacology
|August 23, 2011
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Summary

Morphine dependence disrupts normal lymphocyte (immune cell) movement, causing chaotic trafficking throughout the body and into the central nervous system (CNS). Naltrexone blocked these effects, and morphine worsened CNS infiltration during neuroinflammation.

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Area of Science:

  • Immunology
  • Neuroscience
  • Pharmacology

Background:

  • Opioids, particularly morphine, are known to alter lymphocyte function and immune responses.
  • While morphine's effects on lymphocyte activation are studied, its impact on lymphocyte trafficking remains largely unknown.
  • Understanding lymphocyte migration is crucial for immune surveillance and response, especially in the central nervous system (CNS).

Purpose of the Study:

  • To investigate the effects of morphine dependence on splenocyte (a type of lymphocyte) trafficking in vivo.
  • To determine if morphine alters splenocyte migration patterns in a naive state or during neuroinflammation.
  • To assess the role of the opioid antagonist naltrexone in modulating morphine-induced trafficking changes.

Main Methods:

  • Utilized in vivo bioluminescent imaging to track firefly luciferase transgenic splenocytes.
  • Induced neuroinflammation via intracerebral administration of an IFN-γ DNA plasmid in morphine-dependent and placebo mice.
  • Administered morphine or placebo, followed by adoptive transfer of splenocytes and subsequent imaging.

Main Results:

  • Morphine dependence significantly impaired splenocytes' ability to home to the spleen, causing widespread, non-directed trafficking.
  • Morphine-induced aberrant trafficking, including into the CNS, was reversed by the antagonist naltrexone.
  • Morphine dependence exacerbated splenocyte infiltration into the CNS following induced neuroinflammation.

Conclusions:

  • Morphine dependence severely disrupts normal splenocyte homing to the spleen, leading to extrasplenic and chaotic distribution.
  • Morphine significantly increases lymphocyte infiltration into the CNS, particularly under neuroinflammatory conditions.
  • These findings highlight morphine's profound impact on immune cell migration and CNS entry.