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Eugen Faist
Researcher at Ludwig Maximilian University of Munich
Publications - 117
Citations - 9140
Eugen Faist is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Sepsis & Cytokine. The author has an hindex of 36, co-authored 117 publications receiving 8793 citations.
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Journal ArticleDOI
Alarmins MRP8 and MRP14 Induce Stress Tolerance in Phagocytes under Sterile Inflammatory Conditions
Judith Austermann,Judith Friesenhagen,Selina Kathleen Fassl,Beatrix Petersen,Theresa Ortkras,Johanna Burgmann,Katarzyna Barczyk-Kahlert,Eugen Faist,Siegfried Zedler,Sabine Pirr,Christian Rohde,Carsten Müller-Tidow,Maren von Köckritz-Blickwede,Constantin von Kaisenberg,Stefanie B. Flohé,Thomas Ulas,Joachim L. Schultze,Johannes Roth,Thomas Vogl,Dorothee Viemann +19 more
TL;DR: It is demonstrated that the endogenous alarmins MRP8 and MRP14 induce phagocyte hyporesponsiveness via chromatin modifications in a TLR4-dependent manner that results in enhanced survival to septic shock in mice.
Journal ArticleDOI
Functional analysis of monocyte activity through synthesis patterns of proinflammatory cytokines and neopterin in patients in surgical intensive care.
Eugen Faist,Martin Storck,Lothar Hültner,Heinz Redl,Wolfgang Ertel,Alfred Walz,Friedrich W. Schildberg +6 more
TL;DR: The results demonstrate the impairment of the functional capacity of circulating monocytes and that the degree of functional impairment is proportional to the severity of the injury.
Journal ArticleDOI
Inadequate interleukin-2 synthesis and interleukin-2 messenger expression following thermal and mechanical trauma in humans is caused by defective transmembrane signalling.
Eugen Faist,Christian Schinkel,S. Zimmer,Jean-Pierre Kremer,Guide H. Von Donnersmarck,F. W. Schildberg +5 more
TL;DR: The study was performed to further elucidate the mechanisms of dysfunctional T- cell activation following extensive burn and mechanical injuries and to scrutinize if inadequate lymphokine production after trauma is possibly a result of defective transduction of extracellular signals to the T-cell nucleus.
Journal ArticleDOI
An imbalance in T-helper cell subsets alters immune response after cardiac surgery.
TL;DR: Results indicate a significant suppression of TH1-induced cell-mediated immune response following CPB, while TH2-induced response remains normal, which may be helpful for recovery following cardiac surgery by cleaning the body of the byproducts of CPB.
Journal ArticleDOI
Successful restoration of cell-mediated immune response after cardiopulmonary bypass by immunomodulation.
TL;DR: Human lymphocytic interleukin-2 synthesis, which represents the key event among forward regulatory immune mechanisms, can be protected via in vivo immunoaugmentatory therapy and that this therapy can successfully counteract immunosuppressive effects of cardiopulmonary bypass is demonstrated.