Gut bacterial lauroyl tryptamine reduces GPR183-associated inflammatory responses in human macrophages and T cells in vitro

What To Know

This study reports laboratory (in vitro) experiments showing that lauroyl tryptamine (LT), a bacterial metabolite produced by Agathobacter rectalis, can antagonize GPR183 signaling and reduce GPR183-associated inflammatory gene expression in human macrophage and T‑cell culture models.

The authors analyzed human intestinal tissue expression (including single‑cell transcriptomic data) and found elevated GPR183 expression in colonic and rectal tissues from ulcerative colitis patients, and identified monocytes/macrophages, T cells, B cells, and innate lymphoid cells as GPR183‑expressing populations.

In THP‑1 derived macrophages stimulated with LPS, the oxysterol ligand (OHC) increased transcription of IL6, TNFA, and IL1B, and LT reduced those responses. In activated Jurkat T cells LT modestly reduced OHC‑mediated IL2 transcription.

These results are mechanistic and preclinical: they show how a gut microbial metabolite can influence immune signaling via GPR183 in cell models, which helps generate hypotheses about host–microbiota interactions relevant to IBD but does not demonstrate effects in humans.