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Up-regulation of FPR2, a chemotactic receptor for amyloid beta 1-42 (A beta(42)), in murine microglial cells by TNF alpha

  1. Author:
    Cui, Y. H.
    Le, Y.
    Zhang, X.
    Gong, W.
    Abe, K.
    Sun, R.
    Van Damme, J.
    Proost, P.
    Wang, J. M.

  2. Author Address

    NCI, Canc Res Ctr, Mol Immunoregulat Lab, Frederick, MD 21702 USA NCI, Canc Res Ctr, Mol Immunoregulat Lab, Frederick, MD 21702 USA NCI, Canc Res Ctr, Expt Immunol Lab, Frederick, MD 21702 USA NCI, Intramural Res Support Program, SAIC Frederick, Frederick, MD 21702 USA Univ Louvain, Rega Inst, Louvain, Belgium Cui YH NCI, Canc Res Ctr, Mol Immunoregulat Lab, Frederick, MD 21702 USA
    1. Year: 2002
  2. Journal: Neurobiology of Disease
    1. 10
    2. 3
    3. Pages: 366-377
  4. Type of Article: Article
  1. Abstract:

    Human FPRL1 and its mouse homologue FPR2 are functional receptors for several exogenous and host-derived chemotactic peptides, including amyloid 1342 (A)342), a critical pathogenic factor in Alzheimer's disease. We investigated the effect of TNFalpha on the expression and function of FPR2 in mouse microglial cells, a crucial inflammatory cell type in the CNS. Primary murine microglia and a cell line N9 in resting state expressed low levels of FPR2 gene and lacked the response to chemotactic agonists for this receptor. Incubation with TNFa, however, increased microglial expression of FPR2 gene, in association with potent chemotactic responses to FPR2-specific agonists including Abeta(42). The effect of TNFalpha was dependent on the p55 TNFalpha receptor and activation of MAP kinase p38. TNFalpha concomitantly down-regulated microglial response to the chemokine SDF-1alpha. Thus, by selectively up- regulating FPR2 in microglia, TNFalpha has the capacity to amplify host response in inflammatory diseases in the CNS. (C) 2002 Elsevier Science (USA).

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