Philips Cyriac A, Augustine Philip
Department of Translational Hepatology, Monarch Liver Laboratory, The Liver Institute, Center of Excellence in GI Sciences, Rajagiri Hospital, Chunangamvely, Aluva, Ernakulam, Kerala, India.
Department of Gastroenterology and Advanced GI Endoscopy, Center of Excellence in GI Sciences, Rajagiri Hospital, Chunangamvely, Aluva, Ernakulam, Kerala, India.
J Clin Exp Hepatol. 2022 Mar-Apr;12(2):625-638. doi: 10.1016/j.jceh.2021.08.027. Epub 2021 Sep 3.
Gut microbiota and their homeostatic functions are central to the maintenance of the intestinal mucosal barrier. The gut barrier functions as a structural, biological, and immunological barrier, preventing local and systemic invasion and inflammation of pathogenic taxa, resulting in the propagation or causation of organ-specific (liver disease) or systemic diseases (sepsis) in the host. In health, commensal bacteria are involved in regulating pathogenic bacteria, sinister bacterial products, and antigens; and help control and kill pathogenic organisms by secreting antimicrobial metabolites. Gut microbiota also participates in the extraction, synthesis, and absorption of nutrient metabolites, maintains intestinal epithelial integrity and regulates the development, homeostasis, and function of innate and adaptive immune cells. Cirrhosis is associated with local and systemic immune, vascular, and inflammatory changes directly or indirectly linked to perturbations in quality and quantity of intestinal microbiota and intestinal mucosal integrity. Dysbiosis and gut barrier dysfunction are directly involved in the pathogenesis of compensated cirrhosis and the type and severity of complications in decompensated cirrhosis, such as bacterial infections, encephalopathy, extrahepatic organ failure, and progression to acute on chronic liver failure. This paper reviews the normal gut barrier, gut barrier dysfunction, and dysbiosis-associated clinical events in patients with cirrhosis. The role of dietary interventions, antibiotics, prebiotics, probiotics, synbiotics, and healthy donor fecal microbiota transplantation (FMT) to modulate the gut microbiota for improving patient outcomes is further discussed.
肠道微生物群及其稳态功能对于维持肠道黏膜屏障至关重要。肠道屏障作为一种结构、生物和免疫屏障，可防止致病菌群的局部和全身侵袭及炎症反应，从而避免在宿主中引发器官特异性疾病（肝病）或全身性疾病（脓毒症）。在健康状态下，共生细菌参与调节病原菌、有害细菌产物和抗原；并通过分泌抗菌代谢产物来帮助控制和杀灭致病生物。肠道微生物群还参与营养代谢产物的提取、合成和吸收，维持肠道上皮完整性，并调节先天性和适应性免疫细胞的发育、稳态和功能。肝硬化与局部和全身免疫、血管及炎症变化相关，这些变化直接或间接与肠道微生物群的质量和数量以及肠道黏膜完整性的扰动有关。生态失调和肠道屏障功能障碍直接参与代偿期肝硬化的发病机制以及失代偿期肝硬化并发症的类型和严重程度，如细菌感染、肝性脑病、肝外器官衰竭以及进展为慢加急性肝衰竭。本文综述了肝硬化患者的正常肠道屏障、肠道屏障功能障碍以及与生态失调相关的临床事件。还进一步讨论了饮食干预、抗生素、益生元、益生菌、合生元以及健康供体粪便微生物群移植（FMT）在调节肠道微生物群以改善患者预后方面的作用。
