Identification of delta- and mu-type opioid receptors on human and murine dendritic cells

Makarenkova, Valeria P.; Esche, Clemens; Кост, Н. В.; Shurin, Michael R.; Rabin, Bruce S.; Zozulya, A. A.

doi:10.1016/s0165-5728(01)00313-7

Cited by 38 publications

(19 citation statements)

References 48 publications

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“…In the gut, the inhibitory effects of opioids on intestinal motility are believed to be mediated mainly by MOR located in the central nervous system (76,77). However, since MOR is also expressed on various cells in peripheral tissues (11,(78)(79)(80), it may be speculated that there is a modulation of inflammation by peripheral MOR. In our study, the two selective MOR agonists, DALDA and DAMGO, and the MOR antagonist NM were selected for their inability to cross the blood-brain barrier (52)(53)(54).…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory properties of the μ opioid receptor support its use in the treatment of colon inflammation

Philippe¹,

Dubuquoy²,

Groux³

et al. 2003

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

Anti-inflammatory properties of the μ opioid receptor support its use in the treatment of colon inflammation

Philippe¹,

Dubuquoy²,

Groux³

et al. 2003

J. Clin. Invest.

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“…In addition to pathogen components and inflammatory cytokines, DCs respond to a growing number of neuropeptides; for example, calcitonin gene-related peptide inhibits the antigen-presenting capacity of DCs (22,23), substance P enhances nuclear factor kappa B (NF-κB) activation Morphine Reciprocally Regulates IL-10 and IL-12 Production by Monocyte-Derived Human Dendritic Cells and Enhances T Cell Activation (24), and the vasoactive intestinal peptide synergizes with TNF-α to increase IL-12 production and enhance DC maturation (25). Murine DCs have been shown to express functional κ-opioid (26) as well as δ-and μ-opioid (27) receptors. Stimulation with the κ agonist dynorphin suppressed the T cell stimulatory capacity of DCs without affecting antigen uptake or phenotypic maturation (26).…”

Section: Introductionmentioning

confidence: 99%

“…Stimulation with the κ agonist dynorphin suppressed the T cell stimulatory capacity of DCs without affecting antigen uptake or phenotypic maturation (26). Expression of δ-opioid receptor has also been detected on human DCs (27).…”

Section: Introductionmentioning

confidence: 99%

Morphine Reciprocally Regulates IL-10 and IL-12 Production by Monocyte-Derived Human Dendritic Cells and Enhances T Cell Activation

Messmer

Hatsukari

Hitosugi

et al. 2006

Mol Med

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We evaluated the effect of morphine on human dendritic cells (DCs). Interestingly, immature DCs were found to express all 3 (μ, κ, δ) opioid receptors on the cell surface. Chronic morphine treatment (10 -8 to 10 -12 M) during the development of DCs from monocytes augmented LPS-induced upregulation of HLA-DR, CD86, CD80, and CD83 and increased the T cell stimulatory capacity of DCs, which could be inhibited by naloxone, an opioid receptor antagonist. The change in surface phenotype was paralleled by a p38 MAPK-dependent decrease in IL-10 and increase in IL-12 secretion. Our data indicate that morphine exerts an immunostimulatory effect by modulating LPS-induced DC maturation.

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“…These stress hormones have been reported to shift the immune response from Th1 to Th2 by downregulating Th1 cytokine expression [16]. MOR are also expressed on inflammatory cells, including T cells, monocytes/macrophages and dendritic cells [17,18]. The activation of MOR on T cells was reported to induce the differentiation of Th2 cells and a shift from Th1 to Th2 responses [19,20,21].…”

Section: Introductionmentioning

confidence: 99%

The Involvement of µ-Opioid Receptors in the Central Nervous System in the Worsening of Allergic Airway Inflammation by Psychological Stress in Mice

Okuyama

Wada

Sakurada

et al. 2010

Int Arch Allergy Immunol

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Background: Psychological stress has a recognized association with asthma symptoms. However, the mechanisms linking stress to the exacerbation of asthma are not well defined. µ-Opioid receptors (MOR) have been shown to be involved in the shift of the immune system toward a Th2-predominant response caused by psychological stress. Objective: To test the hypothesis that MOR play a role in the worsening of allergic airway inflammation evoked by psychological stress. Methods: Sensitized mice were exposed to restraint stress followed by antigen challenge. The levels of corticosterone and ovalbumin (OVA)-specific IgE in the blood and the levels of inflammatory cells and cytokine contents in bronchoalveolar lavage fluid were compared between stressed and nonstressed mice. The effects of MOR gene deletion and MOR antagonists/agonists were also investigated. Results: Stress exposure was confirmed by an increase in corticosterone levels. Although OVA-specific IgE levels were not significantly different, the numbers of inflammatory cells and Th2 cytokine levels after antigen challenge in stressed mice were significantly higher than in nonstressed mice. MOR gene deletion ameliorated the stress-induced worsening of antigen-induced airway inflammation, and the administration of morphine, a MOR agonist, reproduced the stress-induced antigen-induced airway inflammation. Selective blocking of MOR in the central nervous system (CNS) significantly reduced stress-induced inflammatory exacerbation, but the blocking of peripheral MOR did not. Conclusions: MOR in the CNS are involved in psychological stress-induced aggravation of allergic airway inflammation.

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Identification of delta- and mu-type opioid receptors on human and murine dendritic cells

Cited by 38 publications

References 48 publications

Anti-inflammatory properties of the μ opioid receptor support its use in the treatment of colon inflammation

Anti-inflammatory properties of the μ opioid receptor support its use in the treatment of colon inflammation

Morphine Reciprocally Regulates IL-10 and IL-12 Production by Monocyte-Derived Human Dendritic Cells and Enhances T Cell Activation

The Involvement of µ-Opioid Receptors in the Central Nervous System in the Worsening of Allergic Airway Inflammation by Psychological Stress in Mice

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