Staphylococcus epidermidis biofilms induce lower complement activation in neonates as compared with adults

Background: Staphylococcus epidermidis (SE) is an important cause of late-onset sepsis in neonates. SE frequently produces a polysaccharide intercellular adhesin (PIA) biofilm, important in the pathogenesis of these infections. Little is known about how the neonatal innate immune system reacts to SE biofilm–associated infections. Our hypothesis was that SE biofilms induce a lower complement activation in neonates as compared with adults. Methods: Cord blood from term infants ( n = 15) and blood from adults ( n = 6) were studied in an ex vivo whole-blood sepsis model. A PIA biofilm–producing strain (SE1457) and its isogenic mutant (M10), producing a non-PIA biofilm, were used. Results: Both SE biofilms induced stronger complement activation in adult than in cord blood ( P ≤ 0.033). We found lower levels of antibodies toward both PIA ( P = 0.002) and the whole bacterium ( P = 0.001) in cord vs. adult blood. By contrast, the interleukin-8 (IL-8) and IL-6 secretion were higher in cord than in adult blood ( P ≤ 0.002). The PIA biofilm induced stronger complement activation than the non-PIA biofilm. Conclusion: We conclude that the neonatal complement system exhibits a maturational deficiency. This may reduce the ability of neonates to combat biofilm-associated SE infections.