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Published on: June 29, 2013
Clara cell protein in full-term pregnancies: the influence of intrauterine growth restriction
Despina D Briana1, Dimitrios Gourgiotis, Maria Boutsikou
1Second Department of Obstetrics and Gynecology, Athens University Medical School, Athens, Greece.
Insights
Intrauterine growth restriction (IUGR) does not affect early Clara cell protein (CC16) levels, suggesting lung immaturity in IUGR neonates isn't due to CC16 deficiency. CC16 levels rise with gestational age, peaking at birth, indicating a role in lung adaptation.
Area of Science:
- Neonatal Physiology
- Pulmonary Medicine
- Biomarker Research
Background:
- Clara cell protein (CC16) is an anti-inflammatory molecule crucial for lung health and a marker of pulmonary epithelial integrity.
- Intrauterine growth restriction (IUGR) is linked to lung structural immaturity and increased respiratory risks in neonates.
Purpose of the Study:
- To compare circulating CC16 concentrations in maternal, fetal, and neonatal samples between IUGR and appropriate-for-gestational-age (AGA) pregnancies.
- To explore the relationship between CC16 levels and gestational age, and other factors like gender, parity, and maternal age.
Main Methods:
- Serum CC16 levels were measured using EIA in 40 mothers and their 20 IUGR and 20 AGA neonates.
- Samples were collected on postnatal days 1 (N1) and 4 (N4).
Main Results:
- No significant differences in CC16 concentrations were found between IUGR and AGA groups.
- Maternal and fetal CC16 levels were lower than neonatal levels (N1 and N4).
- Neonatal CC16 levels increased with gestational age and peaked on day 1 postpartum.
Conclusions:
- Early CC16 deficiency is unlikely to explain lung immaturity or later respiratory issues in IUGR neonates.
- Rising CC16 levels from fetal to neonatal stages suggest a role in fetal lung maturation and adaptation to extrauterine life.
Background:
Clara cell protein (CC16) is an immunomodulatory/anti-inflammatory broncho-alveolar-derived molecule and a biomarker of pulmonary epithelial cells maturity and alveolo-capillary membrane injury. Intrauterine growth-restricted (IUGR) neonates may present with structural lung immaturity, impaired immunocompetence and increased risk for respiratory infections and chronic obstructive lung disease in later life.
Objectives:
To investigate circulating CC16 concentrations in maternal, fetal, and neonatal samples from IUGR and appropriate for gestational age (AGA) pregnancies.
Methods:
Serum CC16 concentrations were determined by EIA in 40 mothers and their 20 IUGR and 20 AGA singleton full-term fetuses-neonates on postnatal days 1 (N1) and 4 (N4).
Results:
No significant differences in CC16 concentrations were observed between IUGR and AGA groups. In both groups, maternal CC16 concentrations were lower compared to N1 and N4 ones (P < 0.001 in each case). Fetal CC16 concentrations were significantly lower compared to N1 and N4 ones (P < 0.001 in each case). In the AGA group, N1 CC16 concentrations were significantly higher than N4 ones (P < 0.001). Combining groups, N1 CC16 concentrations positively correlated with gestational age (r = 0.364, P = 0.021). Finally, the effect of gender, parity, and maternal age on CC16 concentrations was not significant.
Conclusions:
The lack of differences in CC16 concentrations between IUGR and AGA groups possibly suggests that the lung immaturity and later respiratory diseases, associated with the former, may not be related to early CC16 deficiency. CC16 concentrations increase with advancing gestational age and peak on the first day of life, possibly indicating a vital role of the protein in fetal lung maturation and extrauterine pulmonary adaptation.
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