[Increased plasma level of Type I (p55) and Type II (p75) TNF-receptors following trauma]

Excessive synthesis and release of proinflammatory cytokines following trauma have been correlated with poor outcome of injured patients. TNF-alpha seems to play a pivotal role as trigger for the induction of systemic inflammation. Recently, two naturally occurring inhibitors of TNF-alpha, soluble TNF-receptors (sTNFRs) p55 and p75, have been characterized. The present study was undertaken to determine whether severe trauma increases circulating sTNFRs dependent on severity of injury. Injured patients (n = 190) revealed significantly increased plasma levels of both sTNFRs throughout the observation period of 21 days compared to healthy volunteers (n = 125). Patients with severe injury (ISS > 16 pts; n = 130) revealed higher (p < 0.0001) levels of sTNFRs on day of admission than patients with minor trauma (< or = 16 pts; n = 60). Thus, anti-inflammatory mechanisms are activated during the posttraumatic course dependent on severity of injury.