Long-term-impaired expression of nuclear factor-κB and IκBα in peripheral blood mononuclear cells of trauma patients

Nuclear factor (NF)‐κB expression and dimer characteristics were studied in peripheral blood mononuclear cells (PBMCs) of major‐trauma patients and healthy controls. Analysis of PBMCs on days 1, 3, 5, and 10 after trauma revealed that expression of both p65p50 heterodimers and p50p50 homodimers was significantly reduced compared with that in controls. In vitro lipopolysaccharide (LPS) stimulation of PBMCs induced NF‐κB translocation. However, throughout the survey, p65p50 activation remained significantly lower in trauma patients than in controls. After LPS stimulation in vitro, the p65p50/p50p50 ratio was significantly lower in PBMCs from trauma patients than from healthy controls. The ex vivo expression of IκBα was higher in PBMCs of controls than of trauma patients. LPS did not induce IκB expression in PBMCs from trauma patients, but strong induction was obtained with staphylococci, suggesting that this defect is not universal and depends on the nature of the activating signal. Although no direct correlation was found between levels of interleukin‐10 or transforming growth factor‐β and NF‐κB, these immunosuppressive cytokines were significantly elevated in trauma patients by 10 days after admission. The long‐term low‐basal and LPS‐induced nuclear translocation of NF‐κB recalled long‐term immunoparalysis observed in patients with severe inflammatory stress such as trauma.