The purpose of the study is to characterize innate immune function of premature infants, and identify defects that may be responsible for the development of bacterial sepsis.

Sepsis is an important problem in preterm infants and carries a significant morbidity and mortality. It is estimated that 20% of premature infants surviving beyond the first three days of life will have one or more culture-proven bacteremic sepsis. There is increasing epidemiologic and biologic evidence suggesting that preterm newborns are more susceptible to infection than term newborns and adults. Immaturity of the immune system, and, in particular, defects in innate responses to pathogens are of foremost importance in the pathogenesis of neonatal sepsis. The aims of the study are the:

1. Determination of the opsonic capacity of plasma from premature infants, vs. term newborns, and identification possible molecular innate immune defect(s) in preterm plasma.
2. Characterization of the role of TLR2 and TLR4 responses in phagocytes from premature infants using classical TLRs agonists. Determination of the capacity of plasma from premature infants to sustain TLR pathways, with a particular attention paid to the possible role of soluble MD-2 in plasma from premature infants in TLR-dependent opsonophagocytosis.
3. Determine prognostic factors for neonatal sepsis. The identification of a quantitative and/or qualitative defect in innate plasma protein(s) in premature newborns has the potential of identifying those infants who are likely to develop a neonatal sepsis.

Inclusion Criteria:

• Premature or term delivery

Exclusion Criteria:

• none

All premature infants delivered at the University Hospitals of Geneva