PubMed1986
Trauma is known to result in depression of opsonic fibronectin levels as well as abnormalities in neutrophil function. Neutrophil oxidative metabolism, important for bactericidal activity, has not been investigated following injury. Since fibronectin has been reported to increase neutrophil chemiluminescence (CL), we examined the relationship between neutrophil oxidative metabolism (as measured by chemiluminescence) and opsonic fibronectin levels following blunt trauma. Sera from 11 nonseptic and 9 eventually septic-trauma patients were studied. Normal neutrophils incubated in septic-trauma serum had decreased CL responses compared to incubation in nonseptic serum (P less than 0.0001). This difference was apparent immediately after injury, prior to the onset of sepsis. This depression was due to the presence of a serum suppressor of neutrophil chemiluminescence and not to the absence of a serum factor. This suppressor has been partially characterized as a protein of greater than 30,000 Da. Opsonic fibronectin levels were also depressed in septic-trauma sera compared to nonseptic-trauma sera (P less than 0.0001). However, no correlation could be demonstrated between the CL response and opsonic fibronectin levels. Addition of fibronectin to buffer increased the CL response, while addition of fibronectin to nonseptic-trauma serum had no effect. In contrast, addition of fibronectin to septic-trauma sera actually decreased the CL response (P less than 0.05), perhaps by forming complexes with abnormal proteins and interfering with membrane-particle interaction.