Related Experiment Videos
Apoptotic cell death in patients with sepsis, shock, and multiple organ dysfunction
R S Hotchkiss1, P E Swanson, B D Freeman
1Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA. hotch@morpheus.wustl.edu
Critical Care Medicine
|August 14, 1999
Summary
Apoptosis, programmed cell death, is a major cause of cell death in sepsis, particularly affecting lymphocytes. This process, mediated by caspase-3, contributes to the weakened immune response seen in sepsis patients.
Area of Science:
- Immunology
- Cell Biology
- Pathology
Background:
- Sepsis is a life-threatening condition characterized by a dysregulated host response to infection.
- The precise mechanisms of cell death in sepsis, particularly apoptosis, require further elucidation.
- Understanding these mechanisms is crucial for developing targeted therapies.
Purpose of the Study:
- To determine if apoptosis is a primary mechanism of cell death in patients with sepsis.
- To investigate the roles of caspase-3 and BCL-2 in sepsis-induced apoptosis.
Main Methods:
- A prospective study involving 20 sepsis patients who died from multiple organ dysfunction.
- Control groups included critically ill nonseptic patients and normal colon tissue.
- Apoptosis was assessed using hematoxylin and eosin staining, TUNEL assay, and DNA gel electrophoresis.
Main Results:
- Apoptosis was prevalent in various organs of septic patients, notably lymphocytes and intestinal epithelial cells.
- Significant lymphocyte depletion and lymphocytopenia were observed in septic patients.
- Increased caspase-3 activity was detected in septic patients compared to nonseptic controls (p < .01).
Conclusions:
- Caspase-3-mediated apoptosis plays a significant role in lymphocyte loss during sepsis.
- This extensive lymphocyte apoptosis may contribute to the compromised immune function characteristic of sepsis.