ABSTRACT
BACKGROUND AND OBJECTIVES: The risk of transfusion-transmitted bacterial infections as a result of the presence of bacteria in blood is one of the major concerns in transfusion medicine. The purpose of this study was to investigate whether bacteria inoculated into red blood cell concentrates can be inactivated by the INACTINE PEN110 pathogen-reduction process. Four bacterial species were chosen for the study: anaerobic Gram-positive Clostridium perfringens and Propionibacterium acnes, known to be transfusion-transmitted; and two Gram-negative species, Acinetobacter johnsonii and Acinetobacter lwoffii, recently reported to be a common cause of transfusion-associated infections in Europe. MATERIALS AND METHODS: Identical units of leucoreduced red cell concentrates were inoculated with A. johnsonii, A. lwoffii, C. perfringens, or P. acnes. The 4 degrees C control units were put on storage immediately after receiving the spike. The test units were subjected to PEN110 treatment and then stored. The bacterial titre in all units was monitored during a 6-week storage period. RESULTS: The PEN110 inactivation of all tested bacterial strains was time- and titre-dependent. For A. johnsonii and A. lwoffii, no viable bacteria were detected in the units spiked with up to 10(4) colony-forming units (CFU)/ml and treated with PEN110. For red cell units spiked with 10(4)-10(5) CFU/ml of C. perfringens and P. acnes, no viable bacteria were detected in the units treated with PEN110. In control units, there was a gradual decrease in A. johnsonii, A. lwoffii and C. perfringens titres during cold storage, while P. acnes titres remained stable. CONCLUSIONS: The PEN110 pathogen-reduction process was demonstrated to inactivate high titres of A. johnsonii, A. lwoffii, C. perfringens and P. acnes in red cell concentrates.
Subject(s)
Erythrocyte Transfusion , Erythrocytes/drug effects , Erythrocytes/microbiology , Gram-Negative Bacteria/drug effects , Gram-Positive Bacteria/drug effects , Polyamines/pharmacology , Acinetobacter/drug effects , Bacteremia/prevention & control , Bacteremia/transmission , Clostridium perfringens/drug effects , Colony Count, Microbial , Erythrocyte Transfusion/adverse effects , Gram-Negative Bacteria/pathogenicity , Gram-Negative Bacterial Infections/prevention & control , Gram-Negative Bacterial Infections/transmission , Gram-Positive Bacteria/pathogenicity , Gram-Positive Bacterial Infections/prevention & control , Gram-Positive Bacterial Infections/transmission , Humans , In Vitro Techniques , Propionibacterium acnes/drug effects , SafetyABSTRACT
Nitric oxide (NO), delivered by a single addition of S-nitrosoglutathione (GSNO, IC(50) = 60-75 microM), causes the prolonged, multi-day suppression of proliferation of asynchronous, logarithmically growing human (hCASMC, two cell strains), and porcine (porCASMC) coronary artery smooth muscle cells. The inhibition is not cytotoxic, but cytostatic and reversible. Transient exposure (>4-12 h) to GSNO is sufficient to elicit prolonged suppression, but a less than 4 h exposure produces little or no inhibition. Unlike porCASMC and rat and rabbit aortic SMC, hCASMC synthesize little cGMP in response to GSNO stimulation, suggesting loss of NO responsive guanylate cyclase in vitro. The guanylate cyclase inhibitor, ODQ, blocks the slight cGMP synthesis induced by GSNO in hCASMC, but does not prevent GSNO suppression of proliferation. These data support a cGMP independent mechanism for NO induced suppression of hCASMC proliferation which may be significant in the treatment of proliferative coronary artery diseases.
