Dynorphin, a preferential ligand for κ-opioid receptors, is present in nerve fibers and immune cells within inflamed tissue of the rat
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Cited by (81)
Immune cell-mediated opioid analgesia
2020, Immunology LettersCitation Excerpt :Met-ENK was additionally found in proinflammatory, colitogenic Th1 and Th17 lymphocytes in inflamed colon and draining lymph nodes in the chronic colitis [119–121]. DYN was identified in blood and lymph node lymphocytes, and in granulocytes and mononuclear cells in inflamed paws [104,118,122] in the CFA-induced inflammation. The mRNAs of POMC, PENK and PDYN, as well as END and DYN were measured in peritoneal cells comprising neutrophils and monocytes/macrophages in zymosan- or thioglycollate-induced peritoneal inflammation [123,124].
The efficacy of Dynorphin fragments at the κ, μ and δ opioid receptor in transfected HEK cells and in an animal model of unilateral peripheral inflammation
2017, PeptidesCitation Excerpt :Dynorphins are a series of peptides that bind to the κ-opioid receptor (KOP) and mediate anti-nociception peripherally [1,2]. In the periphery, leukocytes have been shown to invade sites of inflammation and release opioid peptides including dynorphin A 1–17, in response to pro-inflammatory interleukin-1β and lipopolysaccharide [3–5]. The opioid receptors μ-opioid receptor (MOP), δ-opioid receptor (DOP) and KOP mediate analgesia both peripherally and centrally and the release of endogenous opioids at the peripheral site of inflammation acts as an endogenous analgesic [6].
Leukocyte opioid receptors mediate analgesia via Ca<sup>2+</sup>-regulated release of opioid peptides
2016, Brain, Behavior, and ImmunityCitation Excerpt :In contrast, the injection of opioid peptide antibodies to tissue devoid of leukocytes (i.e., paws innervated by damaged nerves) did not alter exogenous opioid analgesia. This finding also indicates that endogenous opioids from other sources, for example, peripheral nerves and keratinocytes (Carlton and Coggeshall, 1997; Fell et al., 2014; Hassan et al., 1992; Obara et al., 2009), are not involved. Our experiments with the transfer of immune cells lacking DOR, MOR or KOR clearly show that leukocyte opioid receptors are required for the full manifestation of exogenous opioid analgesia in vivo.
Bi-directional heterologous desensitization between the major HIV-1 co-receptor CXCR4 and the κ-opioid receptor
2008, Journal of NeuroimmunologyCitation Excerpt :While current evidence suggests that dynorphin expression is constitutive in the nervous system, there is evidence that preprodynorphin mRNA expression is inducible through cAMP responsive elements in the preprodynorphin promoter (Messersmith et al., 1994). Furthermore, there is evidence that inflammatory responses in the periphery are accompanied by an accumulation of dynorphin A at both the inflammatory site and in the spinal cord (Hassan et al., 1992; Ruda et al., 1988), and interleukin 1 induces the production of dynorphin A at sites of inflammation (Schafer et al., 1994). Neuroinflammatory conditions would create an environment in which elevated dynorphin would be capable of exerting greater cross-desensitization of CXCR4, potentially disrupting normal neuronal development.
Neuropeptides as signal molecules in common with leukocytes and the hypothalamic-pituitary-adrenal axis
2008, Brain, Behavior, and ImmunityThe expression of prodynorphin gene is down-regulated by activation with lipopolysaccharide in U-937 macrophage cells
2006, Journal of Neuroimmunology