Sepsis, commonly known as blood poisoning, is a disease where the body reacts to a severe infection. During the years, the death toll in sepsis syndromes has increased and has even become higher than in acute myocardial infarctions. Causes for sepsis are diverse. On the one hand, organs and tissue are not sufficiently supplied with blood while on the other hand cells fail to take up sufficient oxygen from the blood. For the clinic, these diverse causes mean that the disease is difficult to diagnose and even harder to treat.
The group from Marcin Osuchowski researches pathological processes that underlie sepsis and septic shock. Thereby, molecular mechanisms are examined, that cause inflammatory response and organ failure occurring in sepsis as well as functional changes and damage in cells and subcellular organelles. Further research emphasis is put on:
- Characterizing various biomarkers and their application for prognostication of developing sepsis syndromes and predicting outcomes in septic patients
- Modeling of the influence of comorbidities (e.g. diabetes), age and/or gender
- Developing and refining appropriate mouse models for sepsis research
One aim is the development and testing of targeted therapeutic strategies aimed at the life-saving modulation of the genomic, humoral and cellular signaling in sepsis syndromes. So far, no EMEA/FDA-approved therapy has been developed that specifically modulates the deranged immune-inflammatory response in sepsis. The research group is therefore working hard to find effective treatment strategies of sepsis syndromes.
Selected Publications
Osuchowski MF, Thiemermann C, & Remick DG. (2016 [Epub ahead of print]). SEPSIS-3 On the Block: What Does It Mean for Pre-Clinical Sepsis Modeling? Shock.
Drechsler S, Weixelbaumer KM, Weidinger A, Raeven P, Khadem A, Redl H, van Griensven M, Bahrami S, Remick D, Kozlov A, & Osuchowski MF. (2015). Why do they die? Comparison of selected aspects of organ injury and dysfunction in mice surviving and dying in acute abdominal sepsis. Intensive Care Med Exp, 3(1):48.
Raeven P, Drechsler S, Weixelbaumer KM, Bastelica D, Peiretti F, Klotz A, Jafarmadar M, Redl H, Bahrami S, Alessi MC, Declerck PJ, & Osuchowski MF. (2014). Systemic inhibition and liver-specific over-expression of PAI-1 failed to improve survival in all-inclusive populations or homogenous cohorts of CLP mice. J Thromb Haemost, 12(6):958-969.
Osuchowski MF, Remick DG, Lederer JA, Lang CH, Aasen AO, Aibiki M, Azevedo LC, Bahrami S, Boros M, Cooney R, Cuzzocrea S, Jiang Y, Junger WG, Hirasawa H, Hotchkiss RS, Li XA, Radermacher P, Redl H, Salomao R, Soebandrio A, Thiemermann C, Vincent JL, Ward P, Yao YM, Yu HP, Zingarelli B, & Chaudry IH. (2014). Abandon the mouse research ship? Not just yet! Shock, 41(6):463-475.
Iskander KN, Osuchowski MF, Stearns-Kurosawa DJ, Kurosawa S, Stepien D, Valentine C, & Remick DG. (2013). Sepsis: multiple abnormalities, heterogeneous responses, and evolving understanding. Physiol Rev, 93(3):1247-1288.
Osuchowski MF, Craciun F, Weixelbaumer KM, Duffy ER, & Remick DG. (2012). Sepsis chronically in MARS: systemic cytokine responses are always mixed regardless of the outcome, magnitude, or phase of sepsis. J Immunol, 189(9):4648-4656.
Drechsler S, Weixelbaumer K, Raeven P, Jafarmadar M, Khadem A, van Griensven M, Bahrami S, & Osuchowski MF. (2012). Relationship between age/gender-induced survival changes and the magnitude of inflammatory activation and organ dysfunction in post-traumatic sepsis. PLoS One, 7(12):e51457.
Weixelbaumer KM, Raeven P, Redl H, van Griensven M, Bahrami S, & Osuchowski MF. (2010). Repetitive low-volume blood sampling method as a feasible monitoring tool in a mouse model of sepsis. Shock, 34(4):420-426.
Osuchowski MF, Connett J, Welch K, Granger J, & Remick DG. (2009). Stratification is the key: inflammatory biomarkers accurately direct immunomodulatory therapy in experimental sepsis. Crit Care Med, 37(5):1567-1573.
Osuchowski MF, Welch K, Siddiqui J, & Remick DG. (2006). Circulating cytokine/inhibitor profiles reshape the understanding of the SIRS/CARS continuum in sepsis and predict mortality. J Immunol, 177(3):1967-1974.