title: Effects of Betaisodona on parameters of host defense.
abstract: The numbers of patients in intensive care units, with immunosuppression, and of elderly people increase in parallel with antibiotic-resistant microorganisms. Therefore the demand for an effective antisepsis increases. Moreover, it became evident that the pathophysiology and the outcome of infection are dependent on the properties of the microorganisms, e.g. synthesis of endo- and exotoxins, and on the host defense, the immune system. In addition to the microbicidal action, we studied the effects of povidone-iodine (PVP-I, Betaisodona) on the generation, release and activity of exotoxins (alpha-hemolysin, phospholipase C, lipase), as well as on granulocyte-derived tissue-destructive enzymes (elastase, beta-glucuronidase) and microbial-induced cytokine generation from human neutrophils. Our results clearly show that PVP-I does not only kill a wide range of bacteria but also inhibits the generation and release of bacterial exotoxins; furthermore, it also inactivates bacterial exotoxins as well as granulocyte-derived tissue-destructive enzymes and cytokines. These data support the usefulness and efficacy of PVP-I as an effective therapeutic agent to combat infection.
authors.affiliation: Institut für Medizinische Mikrobiologie, Otto-von-Guericke-Universität Magdeburg, Germany.
authors.forename: B
authors.initials: B
authors.lastname: König
authors.forename: K
authors.initials: K
authors.lastname: Reimer
authors.forename: W
authors.initials: W
authors.lastname: Fleischer
authors.forename: W
authors.initials: W
authors.lastname: König
mesh_terms: D000368:Aged; D000891:Anti-Infective Agents, Local / Q000008:administration & dosage / Q000494:pharmacology*; D000985:Antisepsis; D001424:Bacterial Infections / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology; D001427:Bacterial Toxins / Q000037:antagonists & inhibitors; D002470:Cell Survival; D003422:Critical Care; D004352:Drug Resistance, Microbial; D004731:Endotoxins / Q000037:antagonists & inhibitors / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004926:Escherichia coli / Q000187:drug effects; D005098:Exotoxins / Q000037:antagonists & inhibitors / Q000502:physiology; D005966:Glucuronidase / Q000037:antagonists & inhibitors / Q000187:drug effects; D006098:Granulocytes / Q000187:drug effects / Q000201:enzymology; D006460:Hemolysin Proteins / Q000187:drug effects; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects*; D016867:Immunocompromised Host; D016209:Interleukin-8 / Q000037:antagonists & inhibitors; D007466:Iodophors / Q000008:administration & dosage / Q000494:pharmacology*; D019272:Leukocyte Elastase / Q000037:antagonists & inhibitors / Q000187:drug effects; D008049:Lipase / Q000187:drug effects; D009504:Neutrophils / Q000187:drug effects; D011206:Povidone-Iodine / Q000008:administration & dosage / Q000494:pharmacology*; D011550:Pseudomonas aeruginosa / Q000187:drug effects / Q000201:enzymology; D013211:Staphylococcus aureus / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000187:drug effects; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000187:drug effects
chemical_list: D000891:Anti-Infective Agents, Local; D001427:Bacterial Toxins; D004731:Endotoxins; D004791:Enzyme Inhibitors; D005098:Exotoxins; D006460:Hemolysin Proteins; D016209:Interleukin-8; D007466:Iodophors; D014409:Tumor Necrosis Factor-alpha; D011206:Povidone-Iodine; D008049:Lipase; D010738:Type C Phospholipases; D005966:Glucuronidase; D019272:Leukocyte Elastase