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Published on: July 24, 2016
Circulating interferon-gamma and white matter brain damage in preterm infants
Ingrid Hansen-Pupp1, Solveig Harling, Ann-Cathrine Berg
1Department of Pediatrics, Lund University Hospital, 221 85 Lund, Sweden. ingrid.pupp@skane.se
Insights
The fetal inflammatory response, particularly elevated interferon-gamma (IFN-gamma) after birth, is linked to white matter brain damage in premature infants. Premature rupture of membranes also correlates with specific inflammatory cytokine patterns.
Area of Science:
- Neonatal immunology
- Perinatal medicine
- Inflammatory response
Background:
- The fetal inflammatory response is implicated in neonatal morbidity.
- Understanding cytokine profiles in premature infants is crucial for predicting outcomes.
Purpose of the Study:
- To evaluate serial circulating cytokine levels in premature infants.
- To correlate cytokine profiles with neonatal morbidities such as white matter brain damage (WMD), intraventricular hemorrhage (IVH), and arterial hypotension.
Main Methods:
- Serial cytokine levels (pro-inflammatory and modulatory) were measured in 74 infants (mean GA 27.1 wk) from cord blood up to 72 hours postnatal.
- Area under the curve (AUC) assessed cytokine burden over time.
- Associations between cytokine levels and morbidities (PROM, WMD, IVH, hypotension) were analyzed.
Main Results:
- Premature rupture of membranes (PROM) associated with increased IL-2, IFN-gamma, and TNF-alpha.
- Elevated postnatal IFN-gamma levels correlated with white matter brain damage (WMD) (OR, 26.0).
- Severe intraventricular hemorrhage (IVH) linked to increased IL-6 and IL-8 AUC (OR, 2.8 and 13.2).
- Arterial hypotension associated with increased IL-6.
Conclusions:
- A fetal immune response, indicated by elevated postnatal IFN-gamma, is associated with WMD development.
- PROM is linked to a T-helper 1 cytokine response.
- The type of inflammatory response is critical for subsequent neonatal morbidity.
Abstract:
The fetal inflammatory response has been suggested as causal in neonatal morbidity. Serial levels of circulating cytokines were evaluated in 74 infants with a mean gestational age (GA) of 27.1 wk. Pro-inflammatory [tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), IL-1 beta, IL-2, IL-6, IL-8, IL-12] [corrected] and modulatory (IL-4, IL-10) cytokines were analyzed from cord blood, and at 6, 24 [corrected] and 72 h postnatal age. Measure of cytokine burden over time was assessed by calculating the area under curve (AUC) for analyzed levels (0-72 h). Premature rupture of membranes (PROM) was associated with higher levels of IL-2 at birth and at 6 h, of IFN-gamma at 6 and 24 h postnatal age and of TNF-alpha at 6 and 24 h. Levels of IFN-gamma at 6, 24, and 72 h were increased in infants developing white matter brain damage (WMD) compared with those without WMD. Infants with arterial hypotension requiring dopamine treatment had an increase in IL-6 with a peak at 6 h of age. Severe intraventricular hemorrhage (IVH) was associated with increase in AUC [(IL-6) and (IL-8), odds ratio (OR) 2.8 and 13.2 respectively], whereas white matter brain damage (WMD) [corrected] was associated with increase in AUC (IFN-gamma; OR, 26.0) [corrected] A fetal immune response with increased postnatal levels of IFN-gamma was associated with development of WMD. PROM was associated with a T-helper 1 cytokine response with increased levels of IFN-gamma. Type of inflammatory response appears of importance for subsequent morbidity.
