The detection of bacterial DNA in serum and ascitic fluid (AF) from patients with liver cirrhosis and ascites is interpreted as molecular evidence of intestinal bacterial translocation (BT) and considered sufficient to activate the cellular immune response leading to greater cytokine synthesis. We studied 34 patients with liver cirrhosis and culture-negative, non-neutrocytic ascites [22 patients without bacterial DNA (group I) and 12 patients with bacterial DNA (group II)]. History and clinical examination were done with the following investigations at first admission and followed up for 24 weeks: serum and AF tumour necrosis factor-alpha (TNF-α), AF polymorphonuclear leukocytes, AF cultivation and detection of blood and AF bacterial DNA. Serum and AF TNF-α were significantly higher in patients with bacterial DNA compared to those without bacterial DNA at first admission [54.5±22.56 vs 35.2±17.97 pg ml−1 (P=0.02) and 123.2±49.32 vs 82.6±29.58 pg ml−1 (P <0.005), respectively]. These changes became highly significant at the end of follow-up of both groups [119.3±27.19 vs 40.2±16.08 pg ml−1 (P <0.001) and 518.8±91.11 vs 97.6±17.81 pg ml−1 (P <0.001), respectively]. In group II, there was a significant increase in serum and AF TNF-α at the end of follow-up compared to at first admission (P <0.001). The relative risk of death, hepatorenal syndrome (HRS) and spontaneous bacterial peritonitis (SBP) was higher in patients with bacterial DNA compared to those without bacterial DNA. We conclude that cirrhotic patients with culture-negative, non-neutrocytic ascites and bacterial DNA have a significantly higher level of serum and AF TNF-α and higher risk of HRS, SBP and mortality compared to those without bacterial DNA, suggesting that bacterial DNA and TNF-α are implicated in these complications of liver cirrhosis.