Gut Microbes and Hepatic Encephalopathy: From the Old Concepts to New Perspectives

Abstract

Hepatic encephalopathy (HE) is a severe complication of advanced liver disease and acute liver failure. The clinical spectrum ranges from minor cognitive dysfunctions to lethargy, depressed consciousness, and coma and significantly impact the quality of life, morbidity, and mortality of the patients. It is commonly accepted that the gut milieu is essential for the development of HE; however, despite intensive research efforts, the pathogenesis of HE is still not fully elucidated. As our knowledge of gut microbiota moves from the pioneering era of culture-dependent studies, the connection between microbes, inflammation, and metabolic pathways in the pathogenesis of HE is becoming increasingly clear, providing exciting therapeutic perspectives. This review will critically examine the latest research findings on the role of gut microbes in the pathophysiological pathways underlying HE. Moreover, currently available therapeutic options and novel treatment strategies are discussed.

Identifying microbe-disease association based on graph convolutional attention network: Case study of liver cirrhosis and epilepsy

“…Over the last decade, increasing researchers pay more attention to the gut-liver-brain axis. The gut-liver-brain axis refers to the bidirectional relationship between the gut and its microbiota, the liver, and the brain, resulting from integrating signals generated by dietary, genetic, and environmental factors ( Rocco et al, 2021 ). Growing evidences have emerged to consider the microbiota-gut-liver-brain axis as a comprehensive approach for better understanding diseases pathophysiology ( Fuenzalida et al, 2021 ).…”

Green Tea Catechin EGCG Ameliorates Thioacetamide‐Induced Hepatic Encephalopathy in Rats via Modulation of the Microbiota‐Gut‐Liver Axis

“…However, the gut environment is altered in patients with HE, resulting in structural and functional dysbiosis of the gut microbiota, decrease numbers of beneficial short‐chain fatty acid (SCFA)‐producing bacteria and increase in the abundance of harmful toxin‐producing bacteria with damaging effects on the intestinal barrier. [ 36 ] Furthermore, due to liver dysfunction and increased intestinal permeability, HE patients are unable to effectively remove gut‐derived toxins (including ammonia and LPS) that penetrate and accumulate in the bloodstream produced by the gut microbiota, which are key factors in inducing the systemic inflammatory response and high blood ammonia in HE. [ 13 ] Increasing researches have suggested that the brain‐gut axis takes on a critical significance in the connection and communication between the brain and the gut, and that both can undergo bidirectional signaling and regulation through neural, endocrine, and Immunity.…”

Exploring the complex interplay: gut microbiome, stress, and leptospirosis

“…The reduction of beneficial autologous taxa leads to decreased production of short-chain fatty acids (SCFAs), resulting in the conversion of primary bile acids into secondary bile acids, which further exacerbates gut dysbiosis, weakens the integrity of the intestinal barrier, reduces gut motility, and promotes small intestinal bacterial overgrowth (SIBO; Rocco et al, 2021 ). These changes amplify the rate of bacterial translocation and promote endotoxemia, introducing a significant amount of pathogen-associated molecular patterns (PAMPs) into the MLNs.…”