Preface - Ous-research.no

Preface - Ous-research.no Preface - Ous-research.no

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Surgical Intensive Care Medicine tively. Plasma levels of several cytokines will be measured by ELISA (multiplex). Furthermore, blood was incubated in a whole blood model. The blood was first anticoagulated with heparin (25 U/mL) and incubated at 37°C with slow rotation in the presence of either Lipopolysaccaride (10 ng/ mL blood), Peptidoglycan isolated form Staphylococcus aureus (1 µg/mL blood) or saline, respectively. At 0,1,4,6,12 and 24 h, plasma was obtained by centrifugation and stored at -70°C. Levels of cytokines will be measured to further assess inflammatory responses after laparoscopic and open surgery. Clinical data are recorded prospectively during hospital stay and at follow-ups 6, 12 and 24 months postoperatively. Determination of P.aeruginosa virulence . Pseudomonas aeruginosa (PAER) is an opportunistic bacterium which seldom cause disease in healthy individuals. But, the increasing number of immunocompromised individuals has provoked a rise in PAER infections. In vitro determination of PAER virulence is complicated, and the current gold standard is a C. elegans killing assay. The killing assay measures relative virulence of PAER serotypes, but a major drawback is that it’s time consuming and resource demanding. In collaboration with Department of Infection Prevention headed by Egil Lingaas, MD, we investigate markers of the innate immune-response as an improved alternative to the established assay. Clinical isolates of PAER from patients with bacteremia were subjected to comparative evaluation in both the established killing assay and a well-established human whole blood model. Due to variation in individual response in human whole blood model we decided to use a cellular model: THP-1 cell line. The viability assay confirmed the differences in virulence of the strains tested on C. elegans, whereas the highly virulent strains for C. elegans reduced significantly the viability of the cells during the assay. The expression of host factors of innate immunological response is currently being investigated to establish a better understanding of host/ pathogen interactions and to identify host factors mediating susceptibility or resistance to virulent PAER isolates Studies on possible effects of a newly developed hemapheresis filter (TM100) on inflammatory mediators and hemodynamic parameters during experimental endotoxinemia in pigs. Therapy in sepsis is still greatly discussed due to a high mortality. Lipopolysaccaride (LPS) is a main initiator of cascade chain reactions during gram negative sepsis that may lead to multi organ failure, circulatory collapse and eventually death. There are some few publications concerning possible positive effects using hemofiltration in humans during severe infections. We have started to test a newly developed hemofiltration filter (TM 100) in anaesthetized pigs during ongoing LPS infusion. Twelve heparinised animals have been used during 2010 to look for an optimal filter content and experimental model. The filter device was placed in the inferior caval vein. We have searched for criteria for possible effects on different parameters. Results so far have revealed a systemic reduction in the TNF-α concentration by 30%. During ongoing hemofiltration an initial drop in systemic blood pressure was detected but could be reversed after intravenous saline. Further studies comparing effects of different hemofiltration systems are planned. The C. elegans killing assays optimized by Reza Assalkhou, PhD, (Dep. of Infection Prevention) showed that this assay is highly reproducible and can differentiate between strains of PAER with high, moderate and low virulence respectively. The ex vivo whole blood model to study the inflammatory response by measurment of the cytokine production of leukocytes was used. Testing blood from 3 different persons clearly indicated the variation in regulation of cytokines production between these persons in response to bacterial infection.( IL (Beta, Ra, 2, 2R, 4, 6, 7, 8, 10, 12, 15), TNF-Alpha, INF-Alpha, INF-Y, GM-CSF, MIP (1Alpha & 1Beta), IP-10, MIG, Eotaxin, RANTES, MCP-1, G-CSF, FGF basic, HGF, VEGF). 12

Surgical Intensive Care Medicine Collaborators: Prof. Heinz Redl, Ludwig-Bolzmann Institute for Traumatology, Vienna, Austria Prof. Soheyl Bahrami, Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria Senior scientist Martin F. Osuchowski, DVM, PhD, Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria Prof. Michael A. Rogy, Vienna, Austria Prof. Christoph Thiemermann, The William Harvey Research Institute, London, UK Prof. Irshad Chaudry, University of Alabama at Birmingham, Birmingham, Alabama, USA Prof. Michael Gallimore, Kent, UK Dr DW. Jones, Kent, UK Prof. Ståle Petter Lyngstadaas, Dept. of Oral Pathology, UiO, Oslo, Norway Prof. Egil Lingaas, Department of Infection Prevention, OUS, Oslo, Norway Dr. Reza Assalkhou, Department of Infection Prevention, OUS, Oslo, Norway 13

Surgical Intensive Care Medicine<br />

Collaborators:<br />

Prof. Heinz Redl, Ludwig-Bolzmann Institute for Traumatology,<br />

Vienna, Austria<br />

Prof. Soheyl Bahrami, Ludwig Boltzmann Institute for Experimental<br />

and Clinical Traumatology, Vienna, Austria<br />

Senior scientist Martin F. Osuchowski, DVM, PhD, Ludwig<br />

Boltzmann Institute for Experimental and Clinical Traumatology,<br />

Vienna, Austria<br />

Prof. Michael A. Rogy, Vienna, Austria<br />

Prof. Christoph Thiemermann, The William Harvey Research<br />

Institute, London, UK<br />

Prof. Irshad Chaudry, University of Alabama at Birmingham,<br />

Birmingham, Alabama, USA<br />

Prof. Michael Gallimore, Kent, UK<br />

Dr DW. Jones, Kent, UK<br />

Prof. Ståle Petter Lyngstadaas, Dept. of Oral Pathology, UiO,<br />

Oslo, Norway<br />

Prof. Egil Lingaas, Department of Infection Prevention, OUS,<br />

Oslo, Norway<br />

Dr. Reza Assalkhou, Department of Infection Prevention,<br />

OUS, Oslo, Norway<br />

13

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