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Updated: Aug 15, 2026
Severe Burn Injury in a Swine Model for Clinical Dressing Assessment
Published on: November 6, 2018
[An experimental study on the apoptosis of PMNs and macrophages during the early postburn stage in severely scalded
1Institucte of Burn Research, Southwestern Hospital, The Third Military Medical University, Chongqing, 400038, P.R. China.
Objective:
To investigate the changes of postburn apoptosis of PMN and the apoptosis of PMN and macrophages after being stimulated by burn sera and the change of the phagocytosis of apoptotic PMNs by macrophages.
Methods:
Rats inflicted by 30% TBSA III degree scalding were employed as the model. PMNs were harvested on the 0, 6, 12 and 24 postburn hour (PBH). Burn sera were harvested at 24 PBHs. PMN apoptosis was detected by flow cytometry. Simultaneously, peritoneal macrophages were collected for the study. The apoptotic change of the macrophages (Mphis) after being stimulated by burn sera and the ability of Mphis phagocytizing apoptotic PMNs at 24 PBHs were examined.
Results:
The PMN apoptosis was obviously inhibited at 6, 12 and 24 PBHs in the scalded rats with no difference between the time spots. Twenty-four hours after being stimulated by burn sera, the apoptotic rate of PMNs on scalded rats was lower than that in normal rats, while the apoptotic rate of Mphis in scalded rats was higher than that in normal rats. The ability of Mphis phagocytizing apoptotic PMNs decreased after severe burn (P < 0.01).
Conclusion:
There exhibited delayed rat PMN apoptosis and decreased ability of the phagocytosis of apoptotic PMNs by the Mphis after severe burn or being stimulated by burn sera. This might lead to the incomplete phagocytosis of apoptotic PMNs by Mphis. As a result, the PMNs would finally come to necrosis and release toxic contents which were important factors in the inducing of SIRS.
Insights
Severe burns delay neutrophil apoptosis and impair macrophage phagocytosis of these cells. This impaired clearance may contribute to systemic inflammatory response syndrome (SIRS) after burn injury.
Area of Science:
- Immunology
- Cell Biology
- Pathophysiology
Context:
- Severe burn injuries trigger complex immune responses.
- Polymorphonuclear neutrophils (PMNs) and macrophages play critical roles in inflammation resolution.
- Apoptosis and phagocytosis are key mechanisms for clearing cellular debris.
Purpose:
- To investigate the impact of severe burns on neutrophil apoptosis.
- To examine the effects of burn serum on neutrophil and macrophage apoptosis.
- To assess the phagocytic capacity of macrophages for apoptotic neutrophils post-burn.
Summary:
- Severe burn injury in rats significantly delayed polymorphonuclear neutrophil (PMN) apoptosis at 6, 12, and 24 postburn hours.
- Burn serum reduced PMN apoptosis but increased macrophage apoptosis compared to normal controls.
- The ability of macrophages to phagocytose apoptotic PMNs was significantly decreased after severe burn.
Impact:
- Delayed PMN apoptosis and reduced phagocytosis by macrophages may lead to incomplete clearance of apoptotic cells.
- Accumulation of uncleared apoptotic PMNs can result in secondary necrosis.
- Release of toxic contents from necrotic PMNs is a potential contributor to Systemic Inflammatory Response Syndrome (SIRS).
