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Characterization of chenodeoxycholic acid as an endogenous antagonist of the G-coupled formyl peptide receptors

  1. Author:
    Chen, X.
    Yang, D.
    Shen, W.
    Dong, H. F.
    Wang, J. M.
    Oppenheim, J. J.
    Howard, O. M. Z.

  2. Author Address

    NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Bld 560, Rm 31-19, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Intraumural Res Support Program, Frederick, MD 21702 USA. Howard OMZ NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Bld 560, Rm 31-19, Frederick, MD 21702 USA.
    1. Year: 2000
  2. Journal: Inflammation Research
    1. 49
    2. 12
    3. Pages: 744-755
  4. Type of Article: Article
  1. Abstract:

    Objective and design: To demonstrate the role of bile acids in immune modulation we examined the ability of select bile acids to inhibit leukocyte migration and chemoattractant receptor function. Materials: To elucidate this mechanism, we employed primary human monocytes, neutrophils and cell lines transfected to express either the high affinity fMLP receptor (FPR) or the low affinity fMLP receptor like 1 (FPRL1). Treatment: Cells were treated with chenodeoxycholic acid (CDCA) and related bile acids in a 0-400 micromolar range. Method: Cell viability, chemotaxis and calcium flux analysis were preformed. Results: We observed that pathophysiological levels (less than or equal to 150 micromolar) of CDCA competitively inhibited H-3-fMLP binding to human monocytes, FPR and FPRL1 transfected cells. Additionally, CDCA reduced both the chemotactic and calcium flux responses induced by fMLP or "W" peptide. Further, CDCA inhibited anti-FPR antibody binding to monocytes. Conclusions: CDCA selectively inhibited human leukocyte chemotaxis and calcium flux induced by fMLP, but not other chemoattractants, suggesting a mechanism for inhibition of inflammation and suppression of innate immune response.

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