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Increased lymphoid tissue apoptosis in baboons with bacteremic shock
Philip A Efron1, Kevin Tinsley, Douglas J Minnich
1Department of Surgery, University of Florida College of Medicine, Gainesville, Florida 32610, USA.
Shock (Augusta, Ga.)
|May 29, 2004
Summary
Sepsis causes early, widespread immune cell death in baboons via multiple pathways. This primate model shows lymphocyte apoptosis mechanisms relevant to human sepsis, aiding therapy development.
Area of Science:
- Immunology
- Cell Biology
- Primate Models
Background:
- Mechanisms of immune cell apoptosis in sepsis are not fully understood.
- Sepsis-induced lymphocyte apoptosis contributes to immune dysfunction.
- Primate models are needed to study sepsis pathogenesis.
Purpose of the Study:
- To investigate molecular mechanisms of immune cell apoptosis during sepsis in primates.
- To determine if baboons are a suitable model for sepsis research.
Main Methods:
- Two baboons received lethal Escherichia coli dose; one control baboon received none.
- Animals were sacrificed at 16 or 24 hours post-septic shock.
- Immunohistochemical staining of lymphoid tissues analyzed lymphocyte apoptosis pathways.
Main Results:
- Septic baboons exhibited marked systemic lymphocyte apoptosis in all lymphoid tissues.
- Apoptosis occurred via both mitochondrial (caspase 9, AIF) and death receptor (Fas ligand) pathways.
- Early and profound lymphocyte death was observed in baboons with gram-negative bacteremia.
Conclusions:
- Gram-negative bacteremia induces early, multifaceted lymphocyte apoptosis in primates.
- The baboon sepsis model effectively replicates human sepsis-induced lymphocyte apoptosis.
- This model is valuable for testing therapies targeting lymphocyte apoptosis in sepsis.