title: Mechanisms of endothelial activation in sepsis and cell culture models to study the heterogeneous host response.
abstract: Sepsis is currently viewed as a fundamental disintegration of control functions from intracellular signalling to immunoregulatory and neuroendocrine mechanisms. The immediate threat in sepsis is invasive infection, and the need to activate immune defense mechanisms to clear the pathogen before irreparable damage occurs. In the process of pathogen elimination, however, the systemic host response to infection may cause collateral damage to the endothelium and may lead to the destruction of host tissues.A number of experimental models have been developed to monitor endothelial activation and to study endothelial dysfunction under septic conditions. Here, we review the application of these models to assess the highly variable host response in sepsis and to investigate the efficacy of adsorbent-based extracorporeal therapies. We also highlight the need for efficient diagnostic tools, which are indispensable to select patients who are likely to benefit from distinct adjunctive therapies.
authors.affiliation: Christian Doppler Laboratory for Innovative Therapy Approaches in Sepsis, Department for Health Sciences and Biomedicine, Danube University Krems, Krems - Austria.
authors.forename: Tanja
authors.initials: T
authors.lastname: Eichhorn
authors.affiliation: Christian Doppler Laboratory for Innovative Therapy Approaches in Sepsis, Department for Health Sciences and Biomedicine, Danube University Krems, Krems - Austria.
authors.forename: Michael B
authors.initials: MB
authors.lastname: Fischer
authors.affiliation: Christian Doppler Laboratory for Innovative Therapy Approaches in Sepsis, Department for Health Sciences and Biomedicine, Danube University Krems, Krems - Austria.
authors.forename: Viktoria
authors.initials: V
authors.lastname: Weber
mesh_terms: D018929:Cell Culture Techniques; D004730:Endothelium, Vascular / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D018805:Sepsis / Q000276:immunology / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology; D051193:Toll-Like Receptors / Q000276:immunology
chemical_list: D051193:Toll-Like Receptors