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Published on: March 2, 2018
Standardized porcine unilateral femoral nailing is associated with changes in PMN activation status, rather than
Michel Paul Johan Teuben1,2,3,4, Roman Pfeifer5,6, Klemens Horst7
1Department of Traumatology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX, Utrecht, The Netherlands. michel.teuben@usz.ch.
Purpose:
Intramedullary nailing (IMN) of fractures is associated with increased rates of inflammatory complications. The pathological mechanism underlying this phenomenon is unclear. However, polymorphonuclear granulocytes (PMNs) seem to play an important role. We hypothesized that a femur fracture and standardized IMN in pigs is associated with altered appearance of PMNs in circulation and enhanced activation status of these cells.
Methods:
A porcine model including a femur fracture and IMN was utilized. Animals were randomized for control [anesthesia + mechanical ventilation only (A/MV)] and intervention [A/MV and unilateral femur fracture (FF) + IMN] conditions. PMN numbers and responsiveness, integrin (CD11b), L-selectin (CD62L) and Fcγ-receptor (CD16 and CD32)-expression levels were measured by flowcytometry of blood samples. Animals were observed for 72 h.
Results:
Circulatory PMN numbers did not differ between groups. Early PMN-responsiveness was retained after insult. PMN-CD11b expression increased significantly upon insult and peaked after 24 h, whereas CD11b in control animals remained unaltered (P = 0.016). PMN-CD16 expression levels in the FF + IMN-group rose gradually over time and were significantly higher compared with control animals, after 48 h (P = 0.016) and 72 h (P = 0.032). PMN-CD62L and CD32 expression did not differ significantly between conditions.
Conclusion:
This study reveals that a femur fracture and subsequent IMN in a controlled setting in pigs is associated with enhanced activation status of circulatory PMNs, preserved PMN-responsiveness and unaltered circulatory PMN-presence. Indicating that monotrauma plus IMN is a specific and substantial stimulus for the cellular immune system. Early alterations of circulatory PMN receptor expression dynamics may be predictive for the intensity of the post traumatic response.
Insights
Intramedullary nailing (IMN) following femur fractures significantly activates circulating polymorphonuclear granulocytes (PMNs). This immune cell activation, indicated by receptor expression changes, suggests IMN is a substantial stimulus for the immune system.
Area of Science:
- Orthopedic Surgery
- Immunology
- Trauma Research
Background:
- Intramedullary nailing (IMN) for fractures is linked to increased inflammatory complications.
- The precise pathological mechanisms remain unclear, but polymorphonuclear granulocytes (PMNs) are implicated.
- Understanding PMN behavior post-IMN is crucial for managing inflammatory responses.
Purpose of the Study:
- To investigate the hypothesis that femur fracture and IMN in pigs alter PMN appearance and activation status in circulation.
- To assess the impact of fracture and IMN on PMN numbers, responsiveness, and receptor expression.
Main Methods:
- A porcine model was used, with animals randomized to control (anesthesia/mechanical ventilation) or intervention (femur fracture + IMN) groups.
- Blood samples were analyzed using flow cytometry to measure PMN numbers, responsiveness, and expression of CD11b, CD62L, CD16, and CD32.
- Animals were observed for 72 hours post-procedure.
Main Results:
- Circulatory PMN numbers and early responsiveness remained unchanged between groups.
- PMN-CD11b expression significantly increased in the fracture + IMN group, peaking at 24 hours.
- PMN-CD16 expression was significantly higher in the fracture + IMN group at 48 and 72 hours compared to controls.
Conclusions:
- Femur fracture with IMN significantly enhances the activation status of circulating PMNs in pigs.
- PMN responsiveness is preserved, and PMN numbers are unaltered, indicating a specific immune stimulus.
- Early changes in PMN receptor expression dynamics may predict the intensity of the post-traumatic inflammatory response.
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