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Sepsis, commonly known as blood poisoning, is a disease where the body reacts to a severe infection. During the years, the death rate 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.

Shock, although of different pathogenesis (hypovolemic, cardiogenic, obstructive, distributive), is associated with minor perfusion and consequently oxygen deficiency of vital organs and tissue hypoxia. Haemorrhages resulting in hypovolemic shock are the common cause of microcirculatory disturbances and oxygenation deficiency in trauma patients.

The group around 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 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 for sepsis syndromes.

Moreover, the Wiggers-Bernard initiative, coordinated by the LBI Trauma, recently published new guidelines for pre-clinical sepsis studies. Until now a large quality gap and confusion with conflicting data, reflecting the variations found in different labs, hampered efficient translation of research into clinics. By implementing the MQTiPSS (Minimum Quality Threshold in Pre-Clinical Sepsis Studies) as best practices, standardization can be brought to pre-clinical models of sepsis worldwide, ultimately improving translation of pre-clinical findings into clinics.





The videos were produced by, and are provided with the written permission of ESICM (European Society of Intensive Care Medicine). The MQTiPSS guidelines are openly accessible in the journals Intensive Care Medicine Experimental (link to the article), Infection and Shock.


Selected Publications

Osuchowski MF, Ayala A, Bahrami S, Bauer M, Boros M, Cavaillon JM, Chaudry IH, Coopersmith CM, Deutschman CS, Drechsler S, Efron P, Frostell C, Fritsch G, Gozdzik W, Hellman J, Huber-Lang M, Inoue S, Knapp S, Kozlov AV, Libert C, Marshall JC, Moldawer LL, Radermacher P, Redl H, Remick DG, Singer M, Thiemermann C, Wang P, Wiersinga WJ, Xiao X, Zingarelli B. (2018). Minimum Quality Threshold in Pre-Clinical Sepsis Studies (Mqtipss): An International Expert Consensus Initiative for Improvement of Animal Modeling in Sepsis. Shock 50(4):377-380.
(free PDF)

Osuchowski MF, Thiemermann C, & Remick DG. (2017). SEPSIS-3 On the Block: What Does It Mean for Pre-Clinical Sepsis Modeling? Shock 47(5):658-660.

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.
(free PDF)

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.

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.
(free full text)

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.
(free PDF)

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.
(free PDF)

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.