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Bacterial infections may constitute an important risk factor of developing cancer disease. Molecular mechanisms by which bacteria contribute to cancer are extremely complex and still remain not fully understood. So far, it is generally accepted that Helicobacter pylori infections are associated with induction of gastric adenocarcinoma and MALT lymphoma. Two H. pylori toxins which modulate many cellular functions are VacA and CagA. So far, CagA is the only one known bacterial oncoprotein. However, many other bacteria produce toxins or effector proteins perturbing host cell homeostasis or/and evoking chronic inflammation. Both processes may be associated with tumour formation. Bacterial toxins which interfere, with various host signal transduction pathways, deregulate processes of cell division, proliferation and differentiation and modulate apoptosis. Some toxins cause even direct DNA damage. This review discuss the potential links between action of bacterial toxins and cancer.

There is an increasing number of evidence of correlation between bacterial infection and atherosclerosis. Heat shock proteins as a possible factor connecting an inflammation reaction inducted by infection and development of the early atherosclerotic lesions is postulated.

TFPI-tissue factor pathway inhibitor appears to play a primary role in regulating TF-induced coagulation. During CAPD procoagulant and anticoagulant activities of the mesothelium are balanced under normal conditions. The aim of the work was to assess TF and TFPI concentrations during peritonitis in CAPD patients. The study was performed in 9 CAPD subjects with peritonitis and 14 clinically stable CAPD patients. TF, total, free and truncated TFPI, thrombomodulin concentrations were measured in plasma and dialysate; C-reactive protein and tumor necrosis factor-TNF alpha were assayed in serum. In 8 patients with S. aureus peritonitis TF and TFPI were not found in dialysate, but were detectable in a case with E. coli peritonitis. C-reactive protein and TNF alpha significantly elevated at the beginning of peritonitis, fell sharply after the therapy. Further studies are needed to establish whether the kind of bacterial peritonitis (Gram-positive or negative) may affect TF and TFPI in plasma and dialysate in CAPD patients.

Significantly higher tissue plasminogen activator activities were found in the abdominal exudate of rats with peritonitis caused by Escherichia coli than in rats with peritonitis caused by Staphylococcus aureus and Candida albicans. The changes of intraabdominal fibrinolysis may be depended on the type of microorganism.