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 (≤150 micromolar) of CDCA competitively inhibited 3H-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 anti body 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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Received 22 June 2000; returned for revision 12 July 2000; accepted by G. Letts 11 August 2000
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Chen, X., Yang, D., Shen, W. et al. Characterization of chenodeoxycholic acid as an endogenous antagonist of the G-coupled formyl peptide receptors. Inflamm. res. 49, 744–755 (2000). https://doi.org/10.1007/s000110050656
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DOI: https://doi.org/10.1007/s000110050656