Prematurity Clinical Trial
Official title:
Defects in Opsonophagocytosis in Premature Infants as a Factor for the Development of Neonatal Sepsis
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.
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Observational Model: Cohort, Time Perspective: Prospective
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