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In vitro studies on PMN-independent endothelial cell damage in trauma: decrease of PMN-endothelial cell adherence by
Abstract:
Trauma favors the development of adult respiratory distress syndrome (ARDS). Adherence of polymorphonuclear leukocytes (PMN) to endothelial cells (EC) with subsequent EC damage by the respiratory burst products and proteases of the PMN is thought to be one of the basic mechanisms in the pathogenesis of ARDS. Recent studies have shown that there might also be PMN-independent mechanisms of EC damage. It would speak for PMN-independent EC damage if in the state of risk for this damage factors were found which decrease PMN activity or if EC damage appeared without PMN. Because in trauma and sepsis pathologic coagulation with high levels of fibrinogen degradation products (FDP) is often diagnosed, we investigated whether FDP-D and FDP-E might influence PMN adherence to EC. We also investigated whether serum of traumatized patients might provoke EC damage in a PMN-independent system in vitro. To achieve this we evaluated the viability of EC using a fluorescence staining method. We found that both FDP-D and FDP-E decreased PMN adherence to human EC significantly (p < 0.01) at a concentration of 50 micrograms/ml. Furthermore we found that EC membrane integrity can be disturbed by serum of trauma patients. These results suggest that in trauma also PMN-independent mechanisms are important for EC damage.
Insights
Trauma can lead to adult respiratory distress syndrome (ARDS). Fibrinogen degradation products (FDP-D and FDP-E) reduce polymorphonuclear leukocyte (PMN) adherence to endothelial cells (EC), suggesting PMN-independent mechanisms in ARDS.
Area of Science:
- Critical Care Medicine
- Immunology
- Pathophysiology
Background:
- Trauma is a significant risk factor for developing adult respiratory distress syndrome (ARDS).
- Polymorphonuclear leukocyte (PMN) adherence to endothelial cells (EC) and subsequent damage by PMN products are considered key mechanisms in ARDS pathogenesis.
- Emerging evidence suggests that PMN-independent pathways may also contribute to EC damage in trauma-associated ARDS.
Purpose of the Study:
- To investigate the influence of fibrinogen degradation products (FDP-D and FDP-E) on PMN adherence to EC.
- To determine if serum from trauma patients can induce EC damage independently of PMNs.
Main Methods:
- In vitro assessment of PMN adherence to human EC.
- Evaluation of EC viability using fluorescence staining.
- Analysis of EC damage induced by serum from trauma patients.
Main Results:
- Both FDP-D and FDP-E significantly decreased PMN adherence to EC at a concentration of 50 µg/ml (p < 0.01).
- Serum from trauma patients was found to disrupt EC membrane integrity in a PMN-independent manner.
- These findings indicate a dual role for FDPs and serum factors in trauma-induced EC injury.
Conclusions:
- Fibrinogen degradation products (FDP-D and FDP-E) may play a protective role by reducing PMN adherence to EC.
- PMN-independent mechanisms, potentially involving serum factors, are crucial in the pathogenesis of EC damage following trauma.
- Understanding these pathways is vital for developing targeted therapies for trauma-induced ARDS.