Complement C5a is present in CSF of human newborns and is elevated in association with preterm birth.
Neuroinflammation contributes to developmental brain injury associated with preterm birth, but the mediators that drive it are incompletely understood. Previous studies have shown that complement C5a is present and injurious in the brains of foetal mice exposed to preterm labour. Here, we demonstrate that C5a is present in the cerebrospinal fluid of newborn human infants and that levels are elevated in those born preterm. The difference is not explained by systemic infection. Complement activation in the neonatal brain and its role as a potential therapeutic target in preterm brain injury warrant further study. Activation in the neonatal brain and its role as a potential therapeutic target for preterm brain injury warrants further study.
a MRC Centre for Reproductive Health, University of Edinburgh, Queen's Medical Research Institute , Edinburgh , UK and.
Rozalia
R
Pataky
a MRC Centre for Reproductive Health, University of Edinburgh, Queen's Medical Research Institute , Edinburgh , UK and.
Forbes A
FA
Howie
b Department of Women's Health , King's College London, St Thomas' Hospital , London , UK.
Guillermina
G
Girardi
a MRC Centre for Reproductive Health, University of Edinburgh, Queen's Medical Research Institute , Edinburgh , UK and.
James P
JP
Boardman
D016022:Case-Control Studies; D015936:Complement C5a / Q000134:cerebrospinal fluid*; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000134:cerebrospinal fluid*
D015936:Complement C5a
C5a; Preterm infant; brain; complement system; neuroinflammation