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Polymorphonuclear cell priming associated with NF-kB activation in patients with severe injury is partially dependent
Hsin-Chin Shih1, Mu-Shun Huang, Chen-Hsen Lee
1Institute of Emergency and Critical Care Medicine, National Yang-Ming University, Taipei, Taiwan.
Background:
Severe trauma may induce alternations of cytokine response and polymorphonuclear cell (PMN) activity in patients. This study investigated the correlation of plasma migration inhibitory factor (MIF) level and PMN activation after severe injury, and their relationship with clinical outcomes.
Study Design:
A prospective observational study was performed at the emergency department and intensive care unit of a university hospital. Thirty-two severe blunt trauma patients (Injury Severity Score greater than 16) with systemic inflammatory response syndrome (SIRS) were enrolled. Age- and gender-matched healthy persons were the controls. Patient blood samples were obtained within 24 hours of and at 72 hours after injury. PMNs were isolated and measured for NF-kBp65 translocation and respiratory burst. Plasma MIF, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-8, and IL-10 concentrations were measured. Control PMNs were incubated with patient plasma preincubated with anti-MIF antibody or anti-IL-6 antibody; cytokine blockade effects were evaluated.
Results:
Twelve patients developed organ failure. Compared with patients without organ failure, patients with organ failure had lower blood pressure and a higher base deficit on admission, higher NF-kBp65 translocation and respiratory burst of PMNs, and higher plasma MIF (968 ± 246 pg/mL vs 564 ± 299 pg/mL) and IL-6 (202 ± 91 pg/mL vs 119 ± 84 pg/mL) levels within 24 hours after injury. Plasma MIF had significant positive correlation with NF-kB translocation of PMNs within 24 hours of incurring trauma (R = 0.668). The presence of anti-MIF antibody in patients' plasma obtained within 24 hours, but not at 72 hours, after injury could significantly partially block the NF-kBp65 translocation and respiratory activity of PMNs in the controls.
Conclusions:
An early increase of plasma MIF associates with NF-kB translocation and respiratory burst in PMNs of severe trauma patients and correlates with higher morbidity. MIF is one of the important factors responsible for early PMN activation and may provide a target of immunomodulation after injury.
Insights
Early increases in plasma migration inhibitory factor (MIF) in severe trauma patients correlate with polymorphonuclear cell (PMN) activation and higher morbidity, suggesting MIF as a potential immunomodulation target.
Area of Science:
- Immunology
- Trauma Medicine
- Critical Care
Background:
- Severe trauma can alter cytokine responses and polymorphonuclear cell (PMN) activity.
- Investigating the link between plasma migration inhibitory factor (MIF) and PMN activation is crucial for understanding trauma outcomes.
Purpose of the Study:
- To examine the correlation between plasma MIF levels and PMN activation post-severe injury.
- To determine the relationship between MIF, PMN activity, and clinical outcomes in trauma patients.
Main Methods:
- Prospective observational study of 32 severe blunt trauma patients and healthy controls.
- Measured PMN activation (NF-kBp65 translocation, respiratory burst) and plasma cytokines (MIF, TNF-alpha, IL-6, IL-8, IL-10).
- Assessed the effect of anti-MIF and anti-IL-6 antibodies on PMN activity.
Main Results:
- Patients with organ failure showed higher plasma MIF and IL-6 levels within 24 hours post-injury.
- Plasma MIF positively correlated with PMN NF-kBp65 translocation (R=0.668) within 24 hours.
- Anti-MIF antibody partially blocked PMN activation in vitro, indicating MIF's role.
Conclusions:
- Early elevation of plasma MIF is linked to PMN activation and increased morbidity in severe trauma.
- MIF plays a significant role in early PMN activation following trauma.
- MIF represents a potential therapeutic target for immunomodulation in trauma care.
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