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Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method
Published on: September 16, 2017
Morphine inhibits the release of tumor necrosis factor in human peripheral blood mononuclear cell cultures
C C Chao1, T W Molitor, K Close
1Neuroimmunobiology and Host Defense Laboratory, Minneapolis Medical Research Foundation, Minnesota 55404.
Abstract:
Opiates modulate a variety of immune responses of peripheral blood mononuclear cells (PBMC). When PBMC were treated with morphine for 24 h, cells released less (P < 0.05) bioactive TNF, a cytokine important in host defense, in the following 24-h incubation period when stimulated with lipopolysaccharide and phytohemagglutinin. Morphine alone did not significantly alter the release of TNF from PBMC cultures. Pretreatment of PBMC cultures for 1 h with naloxone blocked (P < 0.05) the inhibitory effect of morphine on the release of TNF upon stimulation with phytohemagglutinin, but not with lipopolysaccharide, suggesting the involvement of an opioid receptor. The mechanism of morphine-induced suppression of TNF release appears to be counteracted by the effect of this opiate on the release of transforming growth factor (TGF)-beta, since antibodies to this immunoregulatory cytokine further enhanced morphine-related inhibition of TNF release. Taken together, these findings indicate that morphine suppresses the release of bioactive TNF from PBMC and that TGF-beta plays a modulatory role in this inhibitory process.
Insights
Morphine suppresses tumor necrosis factor (TNF) release from immune cells. This effect involves opioid receptors and is modulated by transforming growth factor-beta (TGF-beta), impacting host defense mechanisms.
Area of Science:
- Immunology
- Pharmacology
- Cell Biology
Background:
- Opiates are known to influence various immune cell functions.
- Peripheral blood mononuclear cells (PBMC) play a crucial role in immune responses.
- Tumor necrosis factor (TNF) is a key cytokine involved in host defense.
Purpose of the Study:
- To investigate the effect of morphine on TNF release from PBMC.
- To explore the role of opioid receptors and TGF-beta in morphine's immunomodulatory effects.
Main Methods:
- PBMC were treated with morphine and subsequently stimulated with lipopolysaccharide (LPS) and phytohemagglutinin (PHA).
- Naloxone, an opioid receptor antagonist, was used to assess receptor involvement.
- Antibodies to TGF-beta were employed to investigate its modulatory role.
Main Results:
- Morphine treatment significantly reduced bioactive TNF release from stimulated PBMC.
- Naloxone blocked morphine's inhibitory effect on TNF release stimulated by PHA, but not LPS, indicating opioid receptor involvement.
- Antibodies to TGF-beta enhanced morphine's suppressive effect on TNF release, highlighting TGF-beta's modulatory role.
Conclusions:
- Morphine suppresses the release of bioactive TNF from PBMC.
- Opioid receptors are implicated in morphine's inhibitory action on TNF release.
- Transforming growth factor-beta (TGF-beta) plays a significant modulatory role in this immunosuppressive process.
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