Tessier Mary Elizabeth M, Shneider Benjamin L, Petrosino Joseph F, Preidis Geoffrey A
Section of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Baylor College of Medicine/Texas Children's Hospital, Houston, Texas, USA.
Department of Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
J Pediatr Gastroenterol Nutr. 2025 May;80(5):832-839. doi: 10.1002/jpn3.70014. Epub 2025 Feb 17.
Interactions between the gut microbiome and bile acids are complex and are linked to outcomes in pediatric liver disease by mechanisms that are incompletely understood. In adults, primary bile acids are synthesized in the liver and secreted into the intestine, where complex communities of gut microbes deconjugate, oxidize, epimerize, and 7α-dehydroxylate bile acids into a diverse array of unconjugated, secondary, allo-, iso-, and oxo-bile acids. In contrast, the infant gut microbiota contains a simple, Bifidobacterium-dominant community that transitions to a more diverse, adult-like community as additional microbes colonize the gut. This microbial succession gradually confers deconjugation, oxidation, epimerization, and 7α-dehydroxylation activities that mature the bile acid pool from a profile dominated by primary bile acids early in life to a more diverse, adult-like bile acid profile in later childhood. Altered bile acid profiles in pediatric cholestatic disorders have the potential to change the developmental trajectory of the microbiome. Conversely, alterations in the gut microbiome may re-shape the bile acid pool and hepatic bile acid metabolism. Understanding the mechanisms underlying these interactions will increase our understanding of liver pathophysiology and will motivate new therapeutic strategies for pediatric hepatic disorders. This review aims to highlight differences between the pediatric and adult intestinal microbiome and bile acid pool, and to discuss interactions between gut microbes and bile acids that are critical in early life and that may impact outcomes in infants and children with cholestatic liver disease, including biliary atresia.
肠道微生物群与胆汁酸之间的相互作用十分复杂,其通过尚未完全明确的机制与小儿肝脏疾病的预后相关联。在成年人中,初级胆汁酸在肝脏中合成并分泌到肠道,肠道中复杂的微生物群落会将胆汁酸去共轭、氧化、差向异构化,并进行7α-脱羟基化,使其转化为一系列多样的未共轭、次级、别、异和氧代胆汁酸。相比之下,婴儿肠道微生物群包含一个以双歧杆菌为主的简单群落,随着更多微生物在肠道定殖,该群落会过渡到一个更加多样、类似成人的群落。这种微生物演替逐渐赋予去共轭、氧化、差向异构化和7α-脱羟基化活性,使胆汁酸池从生命早期以初级胆汁酸为主的状态成熟为儿童后期更加多样、类似成人的胆汁酸谱。小儿胆汁淤积性疾病中改变的胆汁酸谱有可能改变微生物群的发育轨迹。相反,肠道微生物群的改变可能会重塑胆汁酸池和肝脏胆汁酸代谢。了解这些相互作用背后的机制将增进我们对肝脏病理生理学的理解,并推动针对小儿肝脏疾病的新治疗策略。本综述旨在强调小儿和成人肠道微生物群及胆汁酸池之间的差异,并讨论肠道微生物与胆汁酸之间在生命早期至关重要且可能影响胆汁淤积性肝病婴儿和儿童(包括胆道闭锁)预后的相互作用。