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IL-4 down-regulates lipopolysaccharide-induced formyl peptide receptor 2 in murine microglial cells by inhibiting the activation of mitogen-activated protein kinases

  1. Author:
    Iribarren, P.
    Cui, Y. H.
    Le, Y.
    Ying, G. G.
    Zhang, X.
    Gong, W. H.
    Wang, J. M.

  2. Author Address

    NCI, Canc Res Ctr, Lab Mol Immunoregulat, Bldg 560,Room 31-40, Frederick, MD 21702 USA NCI, Canc Res Ctr, Expt Immunol Lab, Frederick, MD 21702 USA Lanzhou Mil Med Univ, Biochem Sect, Lanzhou, Peoples R China Lanzhou Mil Med Univ, Mol Immunoregulat Lab, Lanzhou, Peoples R China SAIC Frederick, Basic Res Program, Frederick, MD 21702 USA Wang JM NCI, Canc Res Ctr, Lab Mol Immunoregulat, Bldg 560,Room 31-40, Frederick, MD 21702 USA
    1. Year: 2003
  2. Journal: Journal of Immunology
    1. 171
    2. 10
    3. Pages: 5482-5488
  4. Type of Article: Article
  1. Abstract:

    Microglial cells actively participate in proinflammatory responses in the CNS. Upon stimulation with the bacterial LPS, microglial cells express a functional formyl peptide receptor 2 which mediates the chemotactic and activating effects of a variety of polypeptide agonists including amyloid beta (Abeta(1-42)), a critical pathogenic agent in Alzheimer's disease. In the present study, we found that LPS-induced expression and function of formyl peptide receptor 2 in microglial cells was markedly inhibited by IL-4, a Th2-type cytokine. Our effort to elucidate the mechanistic basis revealed that IL-4 attenuated LPS-stimulated activation of NF- kappaB, extracellular signal-regulated kinase, and p38 mitogen- activated protein kinase, and the effect of IL-4 was associated with a phosphoinositide 3-kinase pathway-dependent increase in serine/threonine phosphatase activity. These results suggest that IL-4 may play an important role in the maintenance of homeostasis of CNS and in the regulation of the disease process characterized by microglial activation in response to proinflammatory stimulants.

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