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Proinflammatory chemokines, such as C-C chemokine ligand 3, desensitize mu-opioid receptors on dorsal root ganglia neurons

  1. Author:
    Zhang, N.
    Rogers, T. J.
    Caterina, M.
    Oppenheim, J. J.

  2. Author Address

    Oppenheim, JJ, NCI, Mol Immunoregulat Lab, Room 21-89A, Frederick, MD 21702 USA NCI, Mol Immunoregulat Lab, Frederick, MD 21702 USA. Temple Univ, Sch Med, Dept Microbiol & Immunol, Philadelphia, PA 19140 USA. Johns Hopkins Univ, Sch Med, Dept Biol Chem & Neurosci, Baltimore, MD 21287 USA.
    1. Year: 2004
  2. Journal: Journal of Immunology
    1. 173
    2. 1
    3. Pages: 594-599
  4. Type of Article: Article
  1. Abstract:

    Pain is one of the hallmarks of inflammation. Opioid receptors mediate antipain responses in both the peripheral nervous system and CNS. In the present study, pretreatment of CCR1:mu-opioid receptor/HEK293 cells with CCL3 (MIP-1alpha) induced internalization of mu-opioid receptors and severely impaired the mu-opioid receptor-mediated inhibition of cAMP accumulation. Immunohistochemical staining showed that CCR1 and mu-opioid receptors were coexpressed on small to medium diameter neurons in rat dorsal root ganglion. Analysis of ligand-induced calcium flux showed that both types of receptors were functional. Pretreatment of neurons with CCL3 exhibited an impaired [D-Ala(2),N-MePhe(4),Gly-o15]enkephalin-elicited calcium response, indicative of the heterologous desensitization of mu-opioid receptors. Other chemokines, such as CCL2, CCL5, and CXCL8, exhibited similar inhibitory effects. Our data indicate that proinflammatory chemokines are capable of desensitizing mu-opioid receptors on peripheral sensory neurons, providing a novel potential mechanism for peripheral inflammation-induced hyperalgesia

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