Soluble Fas Receptor (sFasR) and Fas Ligand (FasL)in Sepsis-Induced Multiple Organ Failure ♦ 191

Fas mediated apoptosis is an important regulatory mechanism in activated immune cells. sFasR can block FasL binding to Fas receptor and inhibit apoptosis in inflammatory cells. We hypothesized that sFasR, but not FasL, would be increased in persistent multiple organ failure (MOF), where continued inflammation has been reported.¹ Plasma from children with sepsis was assayed for sFasR, FasL, IL-10, IL-6 (ELISA) and nitrite/nitrates (Greiss reaction). Children were separated by a daily organ failure index (OFI)¹ into persistent MOF (PMOF=OFI≥3 on day 3); resolved MOF (RMOF=OFI≥3 day 1 or 2, but < 3 by day 3); and No MOF (OFI<3 days 1-3). sFasR was higher in sepsis vs controls (p<.05). sFasR was higher in PMOF vs RMOF and No MOF (p=.005) and in nonsurvivors vs survivors(p=.005). FasL was not higher in sepsis vs controls, or PMOF, but was higher in nonsurvivors (p=.01). sFasR, but not FasL, correlated with plasma IL-10(r_s=.4), IL-6(r_s=.27), and nitrite/nitrates(r_s=.6, all p<.05). In conclusion, sFasR is increased in sepsis, particularly in persistent MOF and nonsurvivors. Increased sFasR, but not FasL, is associated with inflammation in MOF and may perpetuate inflammation by inhibiting apoptosis of activated immune cells.¹ Table

Table 1 No caption available.