Liver disease is correlated with qualitative and quantitative changes in the intestinal microbiota. The alteration in gut microbiota in cirrhotic patients is typified by an overgrowth of potentially pathogenic bacteria, such as Gram-negative species and a decrease in autochthonous familiae. The current study reviewed the features of the complex interaction between gut microbiota and cirrhotic host, the “gut-liver axis”, focussing on the acquired risk of bacterial translocation, systemic inflammation and the relationship with systemic infections in the cirrhotic patient. Elucidating this kind of knowledge might aid in development of novel and innovative approaches for the prevention and therapy of gut dysbiosis and its complication in liver cirrhosis.

Various techniques such as Temporal Temperature Gradient Gel Electrophoresis (TTGE), Real-time PCR and the recent pyrosequencing, have shown evidence that patients suffering from chronic liver disease could exhibit an unbalanced gut microbiota composition. Moreover, it has been observed that cirrhotic patients are prone to a higher risk of dysbiosis due to numerous pathological interactions between the liver and the gastrointestinal tract. Various factors are implicated in the disruption of control of bacterial intestinal growth in patients with cirrhosis, which include namely; alteration in intestinal motility, the higher gastric pH and the reduced bile acid concentration in the colon. The clinical consequences of this failure in the cirrhotic host are characterized by the occurrence of pathological bacterial translocation, a higher risk of intestinal bacterial infections and the risk of decompensation of liver disease.

In situations like drug-induced hypochlorhydria, Helicobacter Pylori colonization, autoimmune atrophic gastritis, gastric surgery, which is typified by failure of  gastric acid barrier, , oropharyngeal flora including mainly Gram-positive bacteria increases in the stomach, duodenum and proximal jejunum. Simultaneously, when the intestinal clearance is impaired because of reduction of small bowel motility, the concentration of the colonic flora increases in the small intestine. 

Although the pathogenesis of the decreased intestinal motility in cirrhotic patients is not yet fully understood, it is hypothesised to be multifactorial and the chief mechanism implicated is the presence of an autonomic neuropathy that play an important role in the delayed oro-cecal transit time (OCTT). In addition, beta-blockers improve intestinal motility and lower intestinal permeability, which in turn, may decrease the small intestinal bacterial overgrowth (SIBO) and decrease the rates of spontaneous bacterial peritonitis. The decrease in bile acids entering the intestine enhance the overgrowth of pathogenic and pro-inflammatory members of the microbiome, and reduced concentration of bile acid further reduces energy supply of the bacterial population relying on 7α-dehydroxylation for their collapses.

Studies in experimental animals suggested that the production of secondary bile acids by Clostridium cluster XIVa group of bacteria caused a positive regulation of bile acid synthesis in the liver. The higher concentration of secondary bile acids in the ileum signified a lower concentration of tauro-β-muricholic acid, an inhibitor of hepatic bile acids synthesis, which forms an important interaction between gut microbiota and liver function. Thus, it can be presumed that as severity of cirrhosis progresses, less secondary bile acids reach the large bowel, which further leads to higher risk of bacterial overgrowth in the small bowel resulting in relative abundance of gram-negative members of the oral and gut microbiota.

Source: Giannelli V, Di Gregorio V, Iebba V, et al. Microbiota and the gut-liver axis: bacterial translocation, inflammation and infection in cirrhosis. World J Gastroenterol. 2014;20(45):16795-16810.