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Interleukin 10 and TNF alpha synergistically enhance the expression of the G protein-coupled formylpeptide receptor 2 in microglia

  1. Author:
    Iribarren, P.
    Chen, K.
    Gong, W.
    Cho, E. H.
    Lockett, S.
    Uranchimeg, B.
    Wang, J. M.

  2. Author Address

    Univ Nacl Cordoba, Fac Ciencias Quim, Dept Bioquim Clin, CIBICI CONICET, RA-5000 Cordoba, Argentina. NCI, Ctr Canc Res, Mol Immunoregulat Lab, Frederick, MD 21702 USA. SAIC Frederick, Tumor Hypoxia Lab, Basic Res Program, Frederick, MD 21702 USA. SAIC Frederick, Tumor Hypoxia Lab, Dev Therapeut Program, Frederick, MD 21702 USA. SAIC Frederick, Image Anal Lab, Frederick, MD 21702 USA.;Iribarren, P, Univ Nacl Cordoba, Fac Ciencias Quim, Dept Bioquim Clin, CIBICI CONICET, RA-5000 Cordoba, Argentina.;piribarr@mail.fcq.unc.edu.ar
    1. Year: 2007
    2. Date: Jul
  2. Journal: Neurobiology of Disease
    1. 27
    2. 1
    3. Pages: 90-98
  4. Type of Article: Article
  5. ISSN: 0969-9961
  1. Abstract:

    Microglia are important participants in inflammatory responses in the central nervous system. We previously observed that tumor necrosis factor alpha (TNF alpha) induces the expression of the formylpeptide receptor mFPR2 on microglial cells. This chemoattractant receptor mediates microglial cell chemotaxis in response to a variety of peptides, including amyloid 0 peptide (A beta(42)), a major pathogenic factor in Alzheimer's disease (AD). In search for agents that regulate microglial activation, we unexpectedly found that IL-10 enhanced the expression of mFPR2 on TNF alpha-activated microglia. This was associated with a markedly increased microglial chemotaxis to A beta(42) and its endocytosis via mFPR2. Mechanistic studies revealed that the synergistic effect of IL-10 on TNF alpha-induction of mFPR2 in microglia was dependent on activation of p38 MAPK. Our results suggest that IL-10 may affect the pathogenic process of AD by up-regulating mFPR2 and thus favoring the recognition and internalization of A beta(42) by activated microglial cells. (c) 2007 Elsevier Inc. All rights reserved.

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External Sources

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  2. DOI: 10.1016/j.nbd.2007.04.010
  3. View record in Web of Science®
  4. WOS: 000247860200009

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