tailieunhanh - Báo cáo y học: "Cell death in sepsis: a matter of how, when, and where"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Cell death in sepsis: a matter of how, when, and where. | Available online http content 13 4 173 Commentary Cell death in sepsis a matter of how when and where Heike Bantel1 and Klaus Schulze-Osthoff2 1 Clinic of Gastroenterology Hepatology and Endocrinology Hannover Medical School Carl-Neuberg-Strasse 1 D-30625 Hannover Germany 2Interfaculty Institute for Biochemistry University of Tubingen Hoppe-Seyler-Str. 4 D-72076 Tubingen Germany Corresponding author Heike Bantel Published 31 July 2009 This article is online at http content 13 4 173 2009 BioMed Central Ltd Critical Care 2009 13 173 doi cc7966 See related research by Hofer et al. http content 13 3 R93 Abstract Dysregulated cell death in several tissues is intimately involved in the pathogenesis of sepsis and contributes to multiple organ failure. Whether cell death during sepsis occurs by necrosis or apoptosis may depend on the cell type as well as the disease stage and is therefore a matter of intense debate. While lymphocyte apoptosis contributes to immunosuppression in sepsis recent evidence suggests that necrosis of hepatocytes predominates in septic patients with liver dysfunction and correlates with poor survival. These distinct modes of cell death might have different consequences for the inflammatory response but are also critical for therapeutic interventions and the disease outcome. Understanding the complexity of death processes employing recently available serum biomarkers of cell death could lead to novel therapeutic approaches and assist in the steering of sepsis treatment. Sepsis is the leading cause of morbidity and mortality in critically ill patients in many intensive care units. The pathophysiology of organ failure and death in patients with sepsis remains elusive. Previously it was generally thought that sepsis represented an unbridled immune response with excessive cytokine production. The failure of almost all antiinflammatory agents to improve survival and the finding that