Positive and negative immunomodulation by opioid peptides

Roda, L.Giorgio; Bongiorno, Lucilla; Trani, Eugenia; Urbani, Alessandra; Marini, Mario

doi:10.1016/0192-0561(95)00105-0

Cited by 35 publications

(8 citation statements)

References 124 publications

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“…Modifications of plasma peptide hydrolysis have been linked to the status of the immune system directly [28], or indirectly, via phenomena such as stress or shock that are related to immune functionality [29]. The immunomodulatory role of opioid peptides [15,16] implies, Bongiorno/Marzano/Marini/Roda/Urbani/ Spagnoli moreover, that alterations in their hydrolysis, and thus of their plasma concentration, necessarily modify neuroimmune signaling. In addition, the limited tridimensional structure that is characteristic of small peptides in polar solvent suggests that their enzyme hydrolysis can be relatively nonspecific.…”

Section: Discussionmentioning

confidence: 99%

“…The existence of neuroimmune interactions was recognized in the early 1980s [14]; the role attributed to neuropeptides is that of modulating, rather than eliciting, immune effects [15,16]. Neuroimmune interactions are bidirectional, and the opioid peptides present in plasma, as well as by the adrenal medulla chromaffin cells, are released by immunocompetent cells [17].…”

Section: Introductionmentioning

confidence: 99%

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Age Increases Leucine Enkephalin Hydrolysis in Human Plasma

Bongiorno

Marzano²,

Marini³

et al. 1998

Gerontology

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Background: The existence of age-associated alterations in immune functions and neuropeptides capable of modulating these functions prompted us to advance the hypothesis that the degradation of plasma neuropeptides, specifically opioid peptides, may be altered by aging. Objective: To verify the possible existence of age-induced variations in neuropeptide hydrolysis in human plasma, using leucine enkephalin as the model substrate. Methods: The hydrolysis of leucine enkephalin and the formation of its hydrolysis byproducts in the presence of plasma enzymes were studied by kinetic and chromatographic techniques in a group of elderly individuals and a control group. Results: The results obtained indicate that in elderly individuals the activity of enkephalin-degrading plasma enzymes is greater than in controls. ANOVA analysis of these data indicates that the dependency of the variation of hydrolysis upon the 2 age groups is statistically significant. Increased substrate hydrolysis, and a modified hydrolysis pattern, appear to be associated with increased activity of the enzymes involved, and with different distribution of the individual enzymes within each class, as well as with severely reduced activity of the low molecular weight plasma inhibitors. Conclusion: The combination of the above-mentioned factors appears to define a characteristic hydrolysis pattern for elderly individuals which is different from that found in controls.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Age Increases Leucine Enkephalin Hydrolysis in Human Plasma

Bongiorno

Marzano²,

Marini³

et al. 1998

Gerontology

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“…As stated earlier, the opioids exert their actions by binding to specific membrane-associated receptors located throughout the central and peripheral nervous systems and on various immunocompetent cells [23,24]. Different opioid receptors differ in their affinity for various opioid ligands and in their cellular distribution, although there is a substantial overlap of function as well as distribution.…”

Section: Peptide Concentrationmentioning

confidence: 99%

δ-Opioid Receptor Antagonist Inhibits Immunomodulation by Met-Enkephalin Analogs

Singh¹,

Bajpai²,

Narayan³

et al. 1999

Neuroimmunomodulation

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The methionine-enkephalin (Met-enkephalin, Tyr-Gly- Gly-Phe-Met) analogs Tyr-D-Ala-Gly-MePhe-Met NHC₃H₇- iso (1) and Tyr-D-Ala-Gly-MePhe-Gly-NHC₃H₇-iso (2) have been shown to enhance human T cell proliferation in in vitro treatment. Their immunomodulatory activities were completely blocked by naloxone, an opioid antagonist. Now we demonstrate that a selective δ-opioid receptor antagonist, ICI-174,864, completely blocks enhancement of T cell proliferation by analogs (1) and (2). The T cell-stimulatory effect was only partially inhibited by the µ-receptor-selective antagonist, β-funaltrexamine hydrochloride. The κ-opioid receptor antagonist, nor-binaltorphimine dihydrochloride, showed no effect on T cell-proliferation stimulated by analogs (1) and (2). These observations suggest that analogs (1) and (2) of Met-enkephalin stimulate T cell proliferation predominantly via δ-opioid receptor present on T cells.

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“…ß-Endorphin induces an increment in the production of proinflammatory cytokines by fresh monocytes in cultures, although the dependence of its action on the presence of a suboptimal concentration of bacterial endotoxin, lipopolysaccharide (LPS), remains controversial [15]. Several opioid receptors have been described in immunocompetent cells [12,13,[16][17][18][19]. Opioid ‰ receptor has been described to be involved in the proliferation of peripheral blood lymphocytes [20,21], while Î and Ì selective agonist produced suppression of antibody secretion by murine splenocytes [22].…”

Section: /Pá Ez Pereda/stalla/holsboer/ Arztmentioning

confidence: 99%

“…ACTH also inhibits the interferon-Á (IFN-Á) production [10] and blocks IFN-Á stimulatory action on the tumoricidal activity of macrophages [11]. Several effects of ß-endorphin on the immune system have been described as well, involving cell proliferation, chemotaxis, natural killer activity, and direct effects on cytokine and antibody secretion [12,13]. An enhancement via opioid receptors of IL-1-induced IL-2 production by a lymphoid cell line was reported [14].…”

Section: /Pá Ez Pereda/stalla/holsboer/ Arztmentioning

confidence: 99%

Differential Regulation of Interleukin-1 Receptor Antagonist by Proopiomelanocortin Peptides Adrenocorticotropic Hormone and β-Endorphin

Kovalovsky

Paez-Pereda

Stalla

et al. 1999

Neuroimmunomodulation

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We have previously described the regulation of interleukin-1 receptor antagonist (IL-1ra) protein secretion and expression by IL-1, glucocorticoids and corticotropin-releasing hormone in monocytes in culture. In the present work, we analyze the direct effect of adrenocorticotropic hormone (ACTH) and β-endorphin on the expression and secretion of IL-1ra by human monocytes in culture. ACTH exerted a dose-dependent inhibitory effect on lipopolysaccharide (LPS)-induced IL-1ra production and mRNA expression. Basal IL-1ra levels were not affected by treatment with any ACTH dose. In contrast, on human monocytes, β-endorphin at concentrations as low as 10 pg/ml produced an increase of basal IL-1ra protein secretion and mRNA expression, this effect being reverted by pretreatment with naloxone. No effect of β-endorphin was observed either in IL-1ra mRNA expression or protein secretion when cells were treated with LPS. The different effects of ACTH and β-endorphin could account for their differential contribution to the inflammatory response: while ACTH contributes to the glucocorticoid overall control of the inflammatory response, β-endorphin exerts an inhibitory tone on the resting IL-1 system. Because IL-1ra is essential in setting the level of monocyte and inflammatory response its differential regulation by the HPA axis hormones contributes to regulating the IL-1/inflammatory temporal response.

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Positive and negative immunomodulation by opioid peptides

Cited by 35 publications

References 124 publications

Age Increases Leucine Enkephalin Hydrolysis in Human Plasma

Age Increases Leucine Enkephalin Hydrolysis in Human Plasma

δ-Opioid Receptor Antagonist Inhibits Immunomodulation by Met-Enkephalin Analogs

Differential Regulation of Interleukin-1 Receptor Antagonist by Proopiomelanocortin Peptides Adrenocorticotropic Hormone and β-Endorphin

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