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Cutting edge: Vasoactive intestinal peptide acts as a potent suppressor of inflannnation in vivo by trans-deactivating chemokine receptors

  1. Author:
    Grimm, M. C.
    Newman, R.
    Hassim, Z.
    Cuan, N.
    Connor, S. J.
    Le, Y. Y.
    Wang, J. M.
    Oppenheim, J. J.
    Lloyd, A. R.

  2. Author Address

    St Georges Clin Sch, Dept Med, Kogarah, NSW 2217, Australia Univ New S Wales, Sch Med, Inflammat Res Unit, Sydney, NSW, Australia NCI, Mol Immunoregulat Lab, Frederick, MD 21702 USA St Georges Clin Sch, Dept Med, Kogarah, NSW 2217, Australia Grimm MC St Georges Clin Sch, Dept Med, Kogarah, NSW 2217, Australia
    1. Year: 2003
  2. Journal: Journal of Immunology
    1. 171
    2. 10
    3. Pages: 4990-4994
  4. Type of Article: Article
  1. Abstract:

    Chemokines mediate trafficking of leukocytes to sites of inflammation and immune responses through activation of G protein-coupled receptors, which thereby provide appealing targets for novel anti-inflammatory agents. Vasoactive intestinal peptide (VIP) is an immunosuppressive neurotransmitter. We show that VIP inhibited the function of chemokine receptors on monocytes and CD4(+) T lymphocytes, with impaired chemotaxis and calcium flux in response to the cognate chemokine ligands CXCL12, CCL3, CCL4, and CCL5. This was mediated by VIP receptor type I and was not caused by chemokine receptor internalization. However, VIPcauseddose- dependentphosphorylation of the chemokine receptor CCR5. This trans-deactivation process was studied in a murine model of delayed-type hypersensitivity continuous infusion of VIP resulted in significant abrogation of monocyte and lymphocyte infiltration. Circulating mononuclear cells from VIP-infused mice were unable to respond to chemokines. VIP may provide a novel approach to treatment of inflammatory diseases through inhibition of chemokine-dependent leukocyte recruitment.

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