Complement and contact activation in term neonates after fetal acidosis

Area of Science:

• Neonatal immunology
• Complement system research
• Contact activation pathways

Background:

• Fetal acidosis is a critical condition in newborns, often linked to hypoxic-ischaemic encephalopathy (HIE).
• The complement and contact systems are key components of the innate immune response, involved in inflammation and tissue repair.
• Understanding their activation in neonatal HIE is crucial for developing targeted therapies.

Purpose of the Study:

• To investigate the activation of the complement and contact systems in neonates experiencing fetal acidosis.
• To compare complement and contact activation markers in newborns with and without HIE.

Main Methods:

• Studied 15 term neonates with HIE (umbilical arterial pH < 7.10) and 15 healthy controls (pH > 7.20).
• Assessed complement function, C1-inhibitor activity, and concentrations of C1q, C1-inhibitor, factor B, C3a, C5a, and factor XIIa.
• Utilized kinetic tests, radial immunodiffusion, and enzyme immunoabsorbent assays 22-28 hours post-birth.

Main Results:

• Neonates with fetal acidosis showed decreased complement function, C1q, and factor B levels.
• Significantly increased levels of activated complement products (C3a, C5a) and contact factors (factor XIIa) were observed in the acidosis group.
• No significant differences in C1-inhibitor concentration or activity were found between groups.

Conclusions:

• Complement and contact system activation are evident in newborns with hypoxic-ischaemic encephalopathy.
• This activation generates mediators that can contribute to inflammation and subsequent tissue damage in affected neonates.
• Findings highlight the role of these innate immune pathways in the pathophysiology of neonatal HIE.