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The devastating consequences of hepatic failure include hepatic encephalopathy, a severe, life threatening impairment of neuronal function. Hepatic encephalopathy is caused by impaired hepatic clearance of NH 4   + . Cellular NH 4   +  uptake is accomplished mainly by the Na + ,K + ,2Cl −  cotransporter. Here we show that hepatic clearance of NH 4   +  is impaired in TNFα deficient as well as TNFR1&TNFR2 double knockout mice, which both develop hyperammonemia. Despite impaired hepatic clearance of NH 4   + , TNFα deficient mice and TNFR1 deficient mice were protected against acute ammonia intoxication. While 54% of the wild-type mice and 60% of TNFR2 deficient mice survived an NH 4   +  load, virtually all TNFα deficient mice and TNFR1 deficient mice survived the treatment. Conversely, TNFα treatment of wild type mice sensitized the animals to the toxic effects of an NH 4   +  load. The protection of TNFα-deficient mice against an NH 4   +  load was paralleled by decreased cerebral expression of NKCC1. According to the present observations, inhibition of TNFα formation and/or NKCC1 may be strategies to favorably influence the clinical course of hepatic encephalopathy.

TNFα induced up-regulation of Na+,K+,2Cl− cotransporter NKCC1 in hepatic ammonia clearance and cerebral ammonia toxicity