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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
Apoptosis differs in dendritic cell subsets early after severe trauma
Marcus Maier1, Emanuel V Geiger, Dirk Henrich
1Department of Trauma, Hand and Reconstructive Surgery, Johann Wolfgang Goethe-University, Frankfurt, Germany. Marcus.Maier@kgu.de
Human Immunology
|July 11, 2009
Summary
Severe trauma increases apoptosis in myeloid dendritic cells (MDC), but not plasmacytoid dendritic cells (PDC). Early post-trauma, dendritic cells show increased antiapoptotic mediators, suggesting a compensatory survival response.
Area of Science:
- Immunology
- Cell Biology
- Trauma Research
Background:
- Dendritic cells (DCs) are crucial immune cells.
- The impact of severe trauma on myeloid DC (MDC) and plasmacytoid DC (PDC) apoptosis is not well understood.
- Investigating early post-traumatic immune responses is vital.
Purpose of the Study:
- To determine the effects of severe trauma on MDC and PDC apoptosis.
- To assess the role of pro- and antiapoptotic factors in early post-trauma.
- To compare the apoptotic susceptibility of MDC and PDC after trauma.
Main Methods:
- Blood samples from trauma patients and healthy controls were analyzed on days 1 and 4 post-admission.
- Mononucleated cells were isolated and stimulated with lipopolysaccharide (LPS).
- Apoptosis was measured using annexin-V staining and flow cytometry; gene expression (Caspase-8, FLIP, Bcl-2, Bax, Gadd45) was analyzed via RT-PCR.
Main Results:
- Severe trauma significantly increased MDC apoptosis compared to controls.
- PDC apoptosis remained unaffected by trauma.
- LPS stimulation reduced MDC apoptosis up to day 4 post-trauma, while its effect on PDC was transient (day 1 only).
- The Bcl-2/Bax ratio in DCs increased significantly post-trauma.
Conclusions:
- Peripheral MDCs are more prone to apoptosis following severe trauma than PDCs.
- Early post-trauma, DCs exhibit enhanced activation of antiapoptotic pathways.
- This suggests a compensatory mechanism aimed at prolonging DC survival in the early trauma phase.
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