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Rough-Form Lipopolysaccharide Increases Apoptosis in Human CD4⁺ and CD8⁺ T Lymphocytes
J S Nielsen1, A Larsson1, T Ledet1
1Department of Anesthesiology and Intensive Care Medicine, Aarhus University Hospital, Aarhus, DenmarkDepartment of Biochemical Pathology, Aarhus University Hospitals, Aarhus, DenmarkDepartment of Anaesthesiology and Intensive Care Medicine, Uppsala University, Uppsala, SwedenDepartment of Surgery, University of Zurich Hospital, Zurich, Switzerland.
Rough-form lipopolysaccharide (R-LPS) increases T cell apoptosis more than smooth-form LPS (S-LPS). This finding highlights T cell apoptosis
Area of Science:
- Immunology
- Cell Biology
- Sepsis Pathogenesis
Background:
- Lymphocyte apoptosis contributes to sepsis pathogenesis.
- Rough-form lipopolysaccharide (R-LPS) elicits a stronger immune response than smooth-form LPS (S-LPS).
- The differential apoptosis-inducing capacity of LPS forms in lymphocyte subsets requires investigation.
Purpose of the Study:
- To compare the apoptosis-inducing effects of R-LPS and S-LPS on human lymphocyte subsets.
- To investigate the role of T cell apoptosis in lipopolysaccharide-induced endotoxemia.
Main Methods:
- Human peripheral blood mononuclear cells were stimulated with R-LPS and S-LPS.
- Multicolour flow cytometry was used to assess apoptosis in CD4(+) T cells, CD8(+) T cells, B cells, and NK cells.
- Annexin V/propidium iodide (AV/PI) staining was employed to detect early apoptotic cells.
Main Results:
- R-LPS significantly increased early apoptosis (AV(+) PI(-)) in CD4(+) and CD8(+) T cells compared to S-LPS and unstimulated cells.
- No significant differences in apoptosis were observed for B cells or NK cells between R-LPS and S-LPS.
- Later apoptosis markers (7-AAD and active caspase-3) did not corroborate the AV/PI findings.
Conclusions:
- R-LPS demonstrates a greater capacity to induce T cell apoptosis than S-LPS.
- T cell apoptosis is a critical mechanism in endotoxemia.
- The form of LPS should be considered in endotoxemia research and clinical management of Gram-negative infections.
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