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Transcription Factor NF&kgr;B Expression and Postsurgical Organ Dysfunction

ObjectiveTo examine the role of neutrophil NF&kgr;B activation in organ dysfunction after major surgery. Summary Background DataNF&kgr;B is a transcription factor involved in the signal transduction of many stimuli that may participate in the pathogenesis of sepsis and resultant multiple organ dysfunction syndrome (MODS). It may therefore be a potential target for modulation in the reduction of postsurgical MODS. MethodsTwenty-five patients undergoing major vascular surgery (thoracoabdominal aortic aneurysm repair) were studied. Perioperative levels of neutrophil NF&kgr;B, CD11b, and glutathione were measured. In vitro inhibition experiments using NF&kgr;B inhibitors were also performed. ResultsNo differences in clinical parameters were apparent before surgery between the patients who subsequently developed MODS and those who did not. However, there was a significant difference in preoperative levels of NF&kgr;B between the patients who developed postoperative organ dysfunction and those who did not. There was also a significant preoperative difference between patients who survived surgery and those who did not. Glutathione levels were reduced both in patients who developed MODS and those who did not at the onset of surgery. NF&kgr;B inhibitors suppressed patient plasma-stimulated NF&kgr;B activation in healthy neutrophils. ConclusionsPreoperative neutrophil NF&kgr;B status may be a marker of postoperative outcome after major surgery, and therapy aimed at attenuating neutrophil NF&kgr;B activation may reduce postoperative sepsis and organ dysfunction.