The role of kappa opioid receptors in immune system – An overview (2023)

European Journal of Pharmacology

Volume 933,

15 October 2022

, 175214

Author links open overlay panel, , ,


Opioids are one of the most effective anti-nociceptive agents used in patients with cancer pain or after serious surgery in most countries. The endogenous opioid system participates in pain perception, but recently its role in inflammation was determined. κ-opioid receptors (KOP receptors), a member of the opioid receptor family, are expressed in the central and peripheral nervous system as well as on the surface of different types of immune cells, e.g. T cells, B cells and monocytes. In this review, we focused on the involvement of KOP receptors in the inflammatory process and described their function in a number of conditions in which the immune system plays a key role (e.g. inflammatory bowel disease, arthritis, subarachnoid hemorrhage, vascular dysfunction) and inflammatory pain. We summed up the application of known KOP ligands in pathophysiology and we aimed to shed new light on KOP receptors as important elements during inflammation.


Opioids are effective in pain relief as well as prevention of its recurrence. Conversely, opioid therapy can adversely affect many organs, including the gastrointestinal (GI), cardiovascular, immune, endocrine and central nervous systems.

The mechanism of opioids action is based on their interactions with opioid receptors located on the cell membrane. Four types of opioid receptors (μ - MOP, δ – DOP, κ – KOP and NOP) and different families of the endogenous agonists (endorphins, enkephalins, dynorphins or nociceptin) constitute the endogenous opioid system (EOS) (Liang et al., 2016). Endogenous opioids are formed by a proteolytic cleavage of precursors. The precursor of endorphins is proopiomelanocortin (POMC), preproenkephalin (PENK) is the precursor of leucine (Leu)- and methionine (Met)-enkephalins, dynorphins are produced from preprodynorphin (PDYN), whereas prepronociceptin is a precursor form of nociceptin (Benarroch, 2012). It should be noted that endogenous opioid peptides do not bind specifically to one type of the opioid receptors, but they exert some affinity for other opioid receptors as well (Table 1).

Endogenous opioid peptides are produced in the central nervous system (CNS), enteric neurons, endocrine and immune cells as well as in various glands throughout the body, i.e. pituitary and adrenal glands. Opioid peptides, which are released by immune cells, interact with opioid receptors located on the primary afferent neurons (Joseph et al., 2010).

Many years of research have shown that expression of the opioid receptors is increased during inflammation. So far, literature provided evidence about the role of MOP, DOP and NOP receptors in this field, their involvement has been confirmed in in vitro experiments and numerous animal models, including inflammatory bowel diseases (IBD), arthritis or vascular inflammation (Iwaszkiewicz et al., 2013; Liang et al., 2016; Philippe et al., 2003).

IBD is a chronic immune-mediated disorder, which is divided into two main types: Crohn's disease (CD) and ulcerative colitis (UC), whose detailed etiology is not well known. A 6-7-fold increase in MOP receptor expression was observed in the ileum and colon collected from patients with CD and a 30-fold increase in mRNA MOP receptor in the colon in patients with UC as compared to healthy controls (Philippe et al., 2006). Moreover, DOP receptor expression at mRNA and protein level was increased in the myenteric and submucosal preparations of the inflamed intestine (Pol et al., 2003). In turn, modulation of NOP receptors activity with small molecules has been recognized as a potential approach to treat inflammatory bowel diseases (Alt et al., 2012). Research to date provides an information about the action and role of three opioid receptors, however, another member of this family, namely KOP receptor, is poorly characterized. KOP receptors are expressed in different types of cells (Fig. 1). Stress-induced KOP receptor activation may enhance the analgesic response and modulate depression (Carlezon et al., 2006; McLennan et al., 2008). Furthermore, peripherally restricted KOP receptor agonists selectively reduce pain and itching, as well as mechanical hypersensitivity (Snyder et al., 2018). Nevertheless reports concerning KOP receptor are limited, therefore, in this review, we focused on the involvement of this receptor in the inflammation and pain (Fig. 2).

Recent advances in laboratory techniques have enabled for development of KOP receptor ligands as anti-nociceptive and anti-inflammatory agents. Some of drugs occur naturally and have been used in the traditional medicine and can be obtained from plants i.e. Salvia divinorum (Jones et al., 2016). Selected KOP receptor ligands have been characterized in preclinical and clinical studies and summarized in Table 2.

Section snippets

Kappa opioids receptors affect the immune cells

Response to harmful stimuli such as pathogens, toxic compounds or damaged cells leads to activation of multiple signaling pathways combined with a release of inflammatory cytokines. Inflammation is characterized by the activation of immune and non-immune cells that protect the host by eliminating pathogens and promoting cell/tissue repair and regeneration. Therefore, activation of the immune system is essential to restore homeostasis. Current state of the art suggests that inflammation may

Inflammatory bowel diseases

KOP receptors, localized in the GI tract, are expressed on myenteric and submucosal plexus neurons (Bagnol et al., 1997; Gray et al., 2006). All opioid receptors are expressed by interstitial cells of Cajal where MOP receptor co-localizes with DOP or KOP receptors in the rat GI tract (Gray et al., 2006). In the human colon, KOP receptors are located in excitatory and inhibitory motoneurons (Galligan and Akbarali, 2014).

Some studies indicated the involvement of KOP receptors during intestinal

Inflammatory pain

Pain is an increasingly common problem, affecting a large percentage of the population. In 2019 20.4% of adults in the United States suffered from chronic pain, and in 7.4% of them the pain limited their daily activities or work (referred to as high intensity chronic pain) (Zelaya et al., 2020). Additionally, more than 50% of the Danish patients with arthritis reported a clinically significant pain (Rifbjerg-Madsen et al., 2017). Nowadays, exact mechanisms underlying the pain are still unclear.


KOP receptors are localized on immune cells, e.g. lymphocytes, macrophages, NK cells, and constitute a potential target in inflammatory diseases. Several studies have confirmed the positive effects of KOP receptor modulation in IBD, subarachnoid hemorrhage, joint inflammation and vascular dysfunction.

Current state of knowledge indicates that activation or inhibition of KOP receptors may play a crucial role in pharmacotherapy. The modulation of inflammation by KOP receptors may occur in two

(Video) Therapeutic Potential of Kappa Opioids in Pain And Addiction

Author contribution

AS and MZ provided the overall concept and framework of the manuscript; AS reviewed current knowledge in the field of paper; AS and MZ wrote the manuscript; JF, WM and MZ revised critically the manuscript. All authors read and approved the final version of the manuscript.

Declaration of competing interest

The authors declare no conflict of interest.


Supported by grants from National Science Center #UMO-2019/35/D/NZ7/02830 to MZ and Medical University of Lodz #503/1-156-04/503-11-001-19-00 to JF.

References (93)

  • C. Alicea et al.

    Inhibition of primary murine macrophage cytokine production in vitro following treatment with the K-opioid agonist U50,488H

    J. Neuroimmunol.


  • Q.S. Auh et al.

    Effects of peripheral κ opioid receptor activation on inflammatory mechanical hyperalgesia in male and female rats

    Neurosci. Lett.


  • D. Bagnol et al.

    Cellular localization and distribution of the cloned mu and kappa opioid receptors in rat gastrointestinal tract



  • M.R. Bruchas et al.

    Long-acting κ opioid antagonists disrupt receptor signaling and produce noncompetitive effects by activating c-Jun N-terminal kinase

    J. Biol. Chem.


  • I. Carroll et al.

    Pharmacological properties of JDTic: a novel κ-opioid receptor antagonist

    Eur. J. Pharmacol.


  • N. Cenac et al.

    Induction of intestinal inflammation in mouse by activation of proteinase-activated receptor-2

    Am. J. Pathol.


  • T. Endoh et al.

    Potent antinociceptive effects of TRK-820, a novel κ-opioid receptor agonist

    Life Sci.


  • T. Endoh et al.

    Characterization of the antinociceptive effects of TRK-820 in the rat

    Eur. J. Pharmacol.


  • C. Gavériaux-Ruff et al.

    Enhanced humoral response in kappa-opioid receptor knockout mice

    J. Neuroimmunol.


  • A.C. Gray et al.

    Comparison of opioid receptor distributions in the rat ileum

    Life Sci.


  • L. Guan et al.

    Inhibition of T cell superantigen responses following treatment with the κ-opioid agonist U50,488H

    J. Neuroimmunol.


  • M. Ichinose et al.

    Enhancement of phagocytosis by dynorphin A in mouse peritoneal macrophages

    J. Neuroimmunol.


  • B.M. Kivell et al.

    Salvinorin A analogs and other kappa-opioid receptor compounds as treatments for cocaine abuse

  • G. Missig et al.

    Blockade of kappa-opioid receptors amplifies microglia-mediated inflammatory responses

    Pharmacol. Biochem. Behav.

    (2022 Jan)

  • T. Miyagi et al.

    Opioids suppress chemokine-mediated migration of monkey neutrophils and monocytes - an instant response



  • S.W. Moon et al.

    The contribution of activated peripheral kappa opioid receptors (kORs) in the inflamed knee joint to anti-nociception

    Brain Res.


    (Video) Pharmacology - OPIOIDS (MADE EASY)

  • M. Salaga et al.

    Novel orally available salvinorin a analog PR-38 protects against experimental colitis and reduces abdominal pain in mice by interaction with opioid and cannabinoid receptors

    Biochem. Pharmacol.


  • R.J. Schepers et al.

    Endogenous kappa-opioid receptor systems inhibit hyperalgesia associated with localized peripheral inflammation



  • R.J.F. Schepers et al.

    Inflammation-induced changes in rostral ventromedial medulla mu and kappa opioid receptor mediated antinociception



  • C.L. Schmid et al.

    Functional selectivity of 6′-guanidinonaltrindole (6′-GNTI) at κ-opioid receptors in striatal neurons

    J. Biol. Chem.


  • K. Shahkarami et al.

    Evaluation of dynorphin and kappa-opioid receptor level in the human blood lymphocytes and plasma: possible role as a biomarker in severe opioid use disorder

    Drug Alcohol Depend.


  • J. Sun et al.

    Salvinorin A attenuates early brain injury through PI3K/Akt pathway after subarachnoid hemorrhage in rat

    Brain Res.


  • N. Xu et al.

    Naltrexone (NTX) relieves inflammation in the collagen-induced- arthritis (CIA) rat models through regulating TLR4/NFκB signaling pathway

    Int. Immunopharm.


  • C. Alt et al.

    Nociceptin/orphanin FQ inhibition with SB612111 ameliorates dextran sodium sulfate-induced colitis

    Eur. J. Pharmacol.


  • R.I. Anderson et al.

    Role of the dynorphin/kappa opioid receptor system in the motivational effects of ethanol

    Alcohol Clin. Exp. Res.


  • L. Arendt-Nielsen et al.

    Analgesic efficacy of peripheral κ-opioid receptor agonist CR665 Compared to oxycodone in a multi-modal, multi-tissue experimental human pain model: selective effect on visceral pain



  • T.C. Beck et al.

    Therapeutic potential of kappa opioid agonists



  • S.M. Belkowski et al.

    Detection of К-opioid receptor mRNA in immature T cells

  • E.E. Benarroch

    Endogenous opioid systems: current concepts and clinical correlations



  • J.M. Bidlack

    Detection and function of opioid receptors on cells from the immune system

    Clin. Diagn. Lab. Immunol.


  • J.M. Bidlack et al.

    Opioid receptors and signaling on cells from the immune system

  • M. Camilleri

    Asimadoline, a κ-opioid agonist

    and Visceral Sensation NIH Public Access


  • W.A. Carlezon et al.

    Depressive-like effects of the κ-opioid receptor agonist salvinorin A on behavior and neurochemistry in rats

    J. Pharmacol. Exp. Therapeut.


  • M. Celik et al.

    IL-4 induces M2 macrophages to produce sustained analgesia via opioids

    JCI Insight


  • H. Chen et al.

    Phosphinic derivatives as new dual enkephalin-degrading enzyme inhibitors: synthesis, biological properties, and antinociceptive activities

    J. Med. Chem.


  • L. Chen et al.

    Inflammatory responses and inflammation-associated diseases in organs



    (Video) Opioid receptors and neuroinflammation

  • T.C. Chicre-Alcântara et al.

    Local kappa opioid receptor activation decreases temporomandibular joint inflammation



  • R. Chou et al.

    The effectiveness and risks of long-term opioid therapy for chronic pain: a systematic review for a national institutes of health pathways to prevention workshop

    Ann. Intern. Med.


  • F.Q. Cunha et al.

    Cytokine-mediated inflammatory hyperalgesia limited by interleukin-4

    Br. J. Pharmacol.


  • T.M. Cunha et al.

    Stimulation of peripheral Kappa opioid receptors inhibits inflammatory hyperalgesia via activation of the PI3Kγ/AKT/nNOS/NO signaling pathway

    Mol. Pain


  • M. Delvaux et al.

    Effect of asimadoline, a κ opioid agonist, on pain induced by colonic distension in patients with irritable bowel syndrome

    Aliment. Pharmacol. Ther.


  • S.P. Didion

    Cellular and oxidative mechanisms associated with interleukin-6 signaling in the vasculature

    Int. J. Mol. Sci.


  • J. Dortch-Carnes et al.

    Bremazocine: a κ-opioid agonist with potent analgesic and other pharmacologic properties

    CNS Drug Rev.


  • G. Elliott et al.

    Topical nalfurafine exhibits anti-inflammatory and anti-pruritic effects in a murine model of AD

    J. Dermatol. Sci.


  • J. Fichna et al.

    Salvinorin A has antiinflammatory and antinociceptive effects in experimental models of colitis in mice mediated by KOR and CB1 receptors

    Inflamm. Bowel Dis.


  • J. Fichna et al.

    Salvinorin A inhibits colonic transit and neurogenic ion transport in mice by activating κ-opioid and cannabinoid receptors

    Neuro Gastroenterol. Motil.


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    What is the role of the kappa opioid receptor? ›

    Kappa opioid receptors (KORs) play a critical role in modulating dopamine, serotonin, and glutamate release in the central nervous system. Dynorphin is a peptide neurotrans- mitter processed from its precursor prodynorphin and is the endogenous ligand of the KOR (5).

    What do Kappa and Delta opioid receptors do? ›

    Similar to mu opioid receptors, kappa and delta opioid receptors reside in the periphery, the dorsal root ganglion, the spinal cord, and in supraspinal regions associated with pain modulation. Both delta and kappa opioid agonists have been shown to activate pain inhibitory pathways in the central nervous system.

    What are the effects of kappa opioid receptor agonist? ›

    However, MOA use results in a plethora of well-described side-effects; these include nausea, vomiting, constipation, respiratory depression, addiction, tolerance, and sedation.


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