Faecalibacterium prausnitzii-associated 18β-glycyrrhetinic acid protects against sepsis via ABCC1-mediated suppression of MAPK/NF-κB signaling.

Faecalibacterium prausnitzii is markedly depleted in septic patients, and its metabolite 18β-glycyrrhetinic acid protects mice from cecal ligation and puncture sepsis.

• Why it matters: Sepsis has limited effective therapies, and although gut dysbiosis is linked to susceptibility, the specific protective microbes, metabolites, and host pathways are not well defined.
• What they did: Fecal 16S rRNA sequencing compared septic versus non-septic patients, while mice received oral F. prausnitzii or exogenous 18β-glycyrrhetinic acid; macrophage assays used lipopolysaccharide to test MAPK/NF-κB signaling and ABCC1 involvement.
• The result: 18β-glycyrrhetinic acid reduced pro-inflammatory mediator expression and suppressed MAPK/NF-κB activation, with ABCC1 silencing attenuating these effects and ABCC1 inhibition by probenecid and MK-571 partially reproducing protection.

AI summary of the abstract · may contain errors · not medical advice · read the paper.