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Summary Background Cronobacter spp. is an opportunistic pathogen causing rare but dangerous cases of meningitis, sepsis and urinary tract infection. Phage therapy overcomes antibiotic resistance and represents an alternative approach to standard antimicrobial treatment. There are no published studies on the use of phages against Cronobacter spp. in vivo. The aim of our study was to prove the effects of isolated Cronobacter-specific phages on renal colonization in a model of urinary tract infection in mice. Material/Methods Urinary tract infection was induced by transurethral application of Cronobacter turicensis (1011 CFU/ml). Simultaneously, isolated Cronobacter-specific phages were administered intraperitoneally (1011 PFU/ml). After 24 hours, kidneys and bladder were collected and used for cultivation and analysis of gene expression and oxidative stress markers. Results Phage therapy reduced the number of Cronobacter colonies in the kidney by 70%. Higher levels of malondialdehyde were reduced by phage therapy without affecting the antioxidant status. The expression of pro-inflammatory cytokines tumor necrosis factor-alpha and monocyte chemoattractant protein-1 increased by the infection and was attenuated by phage therapy. Conclusions Phage therapy proved effective in the prevention of ascending renal infection in a murine model of urinary tract infection. Long-term effects and safety of the treatment are currently unknown. Further studies should test phage therapy in other Cronobacter infection models.

Relationship between advanced glycoxidation end products, inflammatory markers/acute-phase reactants, and some autoantibodies in chronic hemodialysis patients. Uremia and dialysis treatment are associated with uncorrected oxidative and carbonyl stress and microinflammation. Elevation of both oxidative/carbonyl stress end products (advanced oxidation protein products (AOPP), advanced glycation end products (AGEs), and advanced lipoperoxidation end products (ALEs), autoantibodies against modified biological structures, and acute-phase reactants (e.g., C-reactive protein [CRP], fibrinogen) seems to take part in the development of various complications, among them accelerated atherosclerosis. These pathogenic mechanisms are supposed to act synergically; nevertheless, oxidative stress shows a closer relationship to inflammation and acute-phase reaction than advanced glycation. Its end product, AOPP, could, thus, represent a biochemical marker of specific importance.