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Introduction Bile acids (BA) are implicated in gastrointestinal (GI) diseases including bile acid diarrhoea, inflammatory bowel disease and colorectal cancer. Despite their established roles in digestion and metabolism, the precise cellular mechanisms underlying host tissue responses to BAs in the colon remain poorly understood. Here, we aim to generate a bile acid receptor expression atlas of the gastrointestinal epithelial barrier using human colonic organoids alongside immune cells key to colonic health and disease.Methods Gene expression of four BA receptors ( TGR5, FXR, PXR, and VDR) was examined in human blood-derived neutrophils (n=5 donors; ± lipopolysaccharide (LPS)), CD14+ monocyte-derived macrophages (n=5 donors; ± 100 ng/mL LPS + 10 µg/mL peptidoglycan), PBMCs (n=5 donors; ± 100 ng/mL LPS), the human mast cell line HMC-1.1 (n=4 repeats; ± 50 nM PMA + 1 μM A23187), and differentiated human colonic organoids as a model of the human gastrointestinal epithelial barrier (n=3 donors).Results All cell types expressed genes for at least 2 BA receptors. TGR5 was expressed by organoids and all immune cells tested with a cycle threshold (Ct) between 31-35/40 cycles. Colonic organoids expressed FXR mRNA (Ct=30), but immune cells did not. PXR expression was also present in colonic organoids (Ct=30) but low or absent across immune cells. VDR was the most abundant BA receptor expressed by colonic organoids, neutrophils, macrophages, and mast cells (Ct=29-30). Inflammatory stimulation resulted in a significant reduction in TGR5 mRNA in PBMCs (p=0.0027) and neutrophils (p=0.0337), while VDR mRNA expression was elevated in inflammatory macrophages (p=0.0091).Conclusion The colonic epithelial barrier and a wide array of immune cells express BA receptors, indicating the capacity for direct bile acid–mediated signalling within the colon. Altered receptor expression under inflammatory conditions suggests a link between bile acid signalling and inflammatory diseases such as IBD. Ongoing studies aim to define the functional consequences of bile acid exposure in gastrointestinal organoids and immune cells in the context of GI diseases.