The bacterial metabolite 2,3-butanediol ameliorates endotoxin-induced acute lung injury in rats.

Widely identified in bacteria, yeasts and human beings, 2,3-butanediol has been studied for decades. This chemical reportedly functions as a neutralization agent to counteract lethal acidification by bacterial growth and as a signaling molecule involved in interactions among insects, and between bacteria and the plant host. While 2,3-butanediol is produced by many pathogenic bacterial species, its significance and effect on mammals remains basically uncharacterized. Herein, we show that gastric intubation of 2,3-butanediol in rats significantly ameliorates acute lung injury (ALI) and the inflammatory responses induced by the bacterial endotoxin lipopolysaccharide (LPS), with an efficacy comparable to that of the polyphenol compound resveratrol. Such effect was further demonstrated to occur via modulation of the NF-kappaB signaling pathway. These results indicate that bacterial metabolite, 2,3-butanediol has a negative regulatory effect on host innate immunity response, suggesting bacteria may use some metabolites for host immune evasion.