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Updated: Jul 6, 2026

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Chronic exposure of human macrophages in vitro to morphine and methadone induces a putative tolerant/dependent state

Manuel Delgado-Vélez1, Ana Lugo-Chinchilla, Luis Lizardo

  • 1Biology Department, University of Puerto Rico, Río Piedras Campus, POB 23360, San Juan, Puerto Rico 00931-3360.

Journal of Neuroimmunology
|April 9, 2008
PubMed

Insights

Opioid exposure affects immune cells. Acute opioid exposure inhibits phagocytosis, while chronic exposure leads to tolerance, but withdrawal causes a prolonged depression in immune cell function.

Area of Science:

  • Immunology
  • Pharmacology
  • Cell Biology

Background:

  • Previous studies indicated acute opioid exposure inhibits phagocytosis in murine macrophages, while chronic exposure induces tolerance.
  • The impact of opioids on human immune cells, particularly monocyte-derived macrophages (hMDM), requires further investigation.

Purpose of the Study:

  • To investigate the effects of acute and chronic morphine and methadone exposure on human monocyte-derived macrophages (hMDM) phagocytosis.
  • To examine the development of tolerance and withdrawal effects on hMDM phagocytic function.

Main Methods:

  • Cultured human monocyte-derived macrophages (hMDM) from control and methadone patient populations were used.
  • Cells were exposed acutely and chronically to morphine and methadone.
  • Phagocytosis assays were performed to assess immune cell function.

Main Results:

  • Acute exposure to morphine and methadone dose-dependently inhibited hMDM phagocytosis.
  • Chronic exposure led to the development of tolerance, normalizing phagocytosis.
  • Opiate withdrawal in tolerized hMDM resulted in a prolonged depression of phagocytosis lasting several hours.

Conclusions:

  • Human monocyte-derived macrophages (hMDM) exhibit similar responses to opioid exposure as murine macrophages.
  • Opioid withdrawal significantly depresses hMDM phagocytic function for an extended period.
  • These findings suggest opioid withdrawal may seriously compromise host defenses in individuals with opioid dependence.

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