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.