Oxidative Burst of Circulating Neutrophils Following Traumatic Brain Injury in Human (original) (raw)
Figure 1
Inflammatory marker concentrations in plasma.
Mean changes in TNF-α (A, B), IL-6 (C, D) and CRP (E, F) in plasma after injury in trauma controls and traumatic brain injury subjects are presented. Concentration is expressed as mean ± SE values and samples are plotted as histograms at times encompassing 6 h-2 weeks after injury. Uninjured subjects (n = 6) (U, open bars) had low concentration of TNF-α, IL-6 and CRP. The concentration of TNF-α, IL-6 and CRP in trauma control (n = 10) (TC, grey bars) subject was significantly increased at 6 h-1 week (for CRP only to 72 hours) and in traumatic brain injury (n = 12) (TBI, black bars) subject was significantly increased at 6 h-2 weeks after injury. In contrast, increases of TNF-α, IL-6 and CRP after TBI were greater than those of TC subjects at throughout the entire observation period. (B, D, F) The patients with traumatic brain injury were divided into severe (STBI, black spots) (n = 5) and moderate (MTBI, white spots) (n = 7) brain injury. The concentration of TNF-α, IL-6 and CRP in TBI subject with STBI and MTBI were plotted as graphs at times encompassing 6 h-2 weeks after injury. Increases of the concentration of TNF-α, IL-6 and CRP from STBI subjects were greater than those from MTBI subjects throughout the entire observation period (from 6 h to 2 weeks after injury). **P<0.01; *P<0.05, significantly different from uninjured by Fisher’s protected t tests. ##P<0.01; #P<0.05, significantly different from trauma controls by Fisher’s protected t tests. **P<0.01; *P<0.05, significantly different from MTBI by Fisher’s protected t tests.