Discordant tumor necrosis factor-α superfamily gene expression in bacterial peritonitis and endotoxemic shock

Background, Tumor necrosis factor-alpha (TNF-alpha) Is a member of a large family of predominantly homotrimeric type II membrane-associated proteins with both proinflammatory and apopiosis-inducing properties. Although TNF-alpha expression has been studied extensively, little is known about the expression of other members of the TNF-alpha superfamily during acute inflammatory processes. Methods, TNF-alpha, Fas ligand (FasL), and TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) messenger RNA (mRNA) expression were examined in liver lung, spleen, and kidney after either a cecal ligation and puncture or endotoxemic shock with use of semiquantitative reverse transcriptase-polymerase chain reaction. Results. Cecal ligation and puncture increased TNF-alpha mRNA in lung and liver (both P < .05) within 3 hours, which was paralleled by increased Fast mRNA. In the spleen TNF-alpha and Fast mRNA significantly declined (both P < .05). In contrast to TNF-alpha and FasL, TRAIL mRNA levels were unchanged in all organs except lung, where if was reduced at 24 hours (P < .05). Endotoxemic shock also increased lung TNF-alpha and Fast mRNA levels (both P < .05). Conclusions, In acute inflammatory processes TNF-alpha and FasL mRNA increase concordantly; in several solid organs. In contrast: TRAIL mRNA levels do not consistently change during these acute inflammatory processes, suggesting that its expression is under independent and discordant regulatory control.