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The syndrome of decreased immunity caused by cirrhosis is a combination of different immunological mechanisms and reactions which result from an advanced stage of the liver disease. The synthesis of proteins of the acute phase becomes impaired, there develop different deficiencies of the complement system, and there ensues a decrease of receptors that are meant to recognize antigens. The negative changes become apparent in the field of cell responses, e.g. there are changes in the amounts of generated monocytes and macrophages, and their phagocytic capabilities and chemotaxic reactions are impacted as well. The humoral response results in distorted synthesis of particular antigen categories. The risk of detrimental immunoresponses with the end result of endotoxemia is not rarely coupled with both local and global infections. The combination of the aforesaid immunodeficiencies worsens the healing chances of cirrhosis sufferers and more often than not it increases the mortality of the affected patients. [ABSTRACT FROM AUTHOR]

Aim of the study: Hepatic encephalopathy and hyperammonemia is a clinical complication associated with liver cirrhosis. The brain is the target organ for ammonia toxicity. Ammonia-induced brain injury is related to oxidative stress, locomotor activity dysfunction, and cognitive deficit, which could lead to permanent brain injury, coma and death if not appropriately managed. There is no promising pharmacological intervention against cirrhosisassociated brain injury. Taurine (TAU) is one of the most abundant amino acids in the human body. Several physiological and pharmacological roles have been attributed to TAU. TAU may act as an antioxidant and is an excellent neuroprotective agent. This study aimed to evaluate the effect of TAU supplementation on cirrhosisassociated locomotor activity disturbances and oxidative stress in the brain. Material and methods: Rats underwent bile duct ligation (BDL) surgery, and plasma and brain ammonia level, plasma biochemical parameters, and rats' locomotor function were monitored. Furthermore, brain tissue markers of oxidative stress were assessed. Results: It was found that plasma and brain ammonia was increased, and markers of liver injury were significantly elevated in the cirrhotic group. Impaired locomotor activity was also evident in BDL rats. Moreover, an increase in brain tissue markers of oxidative stress was detected in the brain of cirrhotic animals. It was found that TAU supplementation (50, 100, and 200 mg/kg, gavage) alleviated brain tissue markers of oxidative stress and improved animals' locomotor activity. Conclusions: These data suggest that TAU is a potential protective agent against cirrhosis-associated brain injury. [ABSTRACT FROM AUTHOR]