A microbiota-dependent bile acid reprograms alveolar macrophages to control lung inflammation

The human microbiota orchestrates immune responses through both local cell-cell interactions and circulating metabolites. While microbiota-derived metabolites are particularly relevant at sites distal to the intestine, most have been described to act locally in the gut, with only a few, such as short-chain fatty acids or aromatic amino acid derivatives, shown to exert systemic effects. 1 In this context, bile acids stand out for their potential to expand this space: although primarily shown to promote Treg cells and inhibit Th17 responses in the gut, 2 microbial transformations generate a structurally diverse pool of bile acid derivatives, providing a rich platform for discovering compounds capable of shaping immunity at distal sites. 2