Journal
INFLAMMATION RESEARCH
Volume 49, Issue 12, Pages 744-755Publisher
SPRINGER BASEL AG
DOI: 10.1007/s000110050656
Keywords
chenodeoxycholic acid; chemotaxis; bile acids; formyl peptide receptor; formyl peptide receptor like 1. calcium flux
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Funding
- NCCIH NIH HHS [Y2-AT-9002] Funding Source: Medline
- NCI NIH HHS [N01-CO-56000] Funding Source: Medline
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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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