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Published on: November 20, 2015
Placental IL-10 dysregulation and association with bronchopulmonary dysplasia risk
Elisabeth C McGowan1, Stefan Kostadinov, Kathryn McLean
1Department of Pediatrics, Women and Infants Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island 02915, USA.
Insights
Bronchopulmonary dysplasia (BPD) in premature infants may be predicted by placental cytokine expression. Lower levels of anti-inflammatory interleukin-10 (IL-10) in the placenta are linked to BPD development, suggesting a protective role.
Area of Science:
- Perinatology
- Neonatology
- Immunology
Background:
- Premature infants often exhibit proinflammatory states, contributing to bronchopulmonary dysplasia (BPD) pathogenesis.
- The placenta's role in initiating BPD events is under investigation.
- Cytokine profiles in amniotic fluid, cord serum, and tracheal aspirates indicate a shift towards inflammation.
Purpose of the Study:
- To investigate placental cytokine expression as a predictor of BPD in premature infants.
- To determine if placental cytokine profiles reflect events leading to BPD development.
- To analyze the association between specific cytokines (IL-6, IL-10) and BPD incidence.
Main Methods:
- Retrospective, case-controlled study of 98 premature infants (49 with BPD, 49 without).
- Matched infants by gender, birth weight, and year of birth.
- Immunohistochemistry used to assess cytokine expression (IL-6, IL-10) in placental tissues, membrane rolls, and umbilical cords.
Main Results:
- Interleukin-6 (IL-6) expression was similar in infants with and without BPD.
- Anti-inflammatory interleukin-10 (IL-10) expression was significantly lower in the placentas of infants who developed BPD.
- Reduced IL-10 expression in the villous trophoblast layer correlated with a significantly lower odds of developing BPD (adjusted OR 0.08).
Conclusions:
- Placental cytokine balance, particularly involving IL-10, is critical for normal lung development in premature infants.
- Lower placental IL-10 expression is associated with an increased risk of BPD.
- IL-10 may play a protective role against the development of BPD.
Abstract:
Cytokine profiles in amniotic fluid, cord serum, and tracheal aspirate of premature infants suggest a shift toward a proinflammatory state. Cytokines also contribute to the pathogenesis of bronchopulmonary dysplasia (BPD). We hypothesize that the initiating events for BPD are reflected in the placenta and propose that placental expression of cytokines provide a blueprint of events leading to BPD. This is a retrospective, case-controlled study of placental cytokines of premature infants with (n = 49) and without (n = 49) BPD, matched for gender, birth weight, and year of birth at Women and Infants Hospital between 2003 and 2005. Cytokine expression, including IL-6 and IL-10, was determined by immunohistochemistry in membrane rolls, umbilical cords, and placentas. IL-6 was similarly expressed in all tissues of infants with and without BPD. In contrast, anti-inflammatory cytokine IL-10 was less prominent in the placenta of patients with BPD compared with those without BPD. IL-10 expression in the villous trophoblast layer was associated with a reduced odds ratio of developing BPD (adjusted OR 0.08, 95% CI 0.01-0.70, p = 0.02). These results suggest that a placental balance between inflammatory and anti-inflammatory cytokines is crucial to normal lung organogenesis. Importantly, IL-10 seems to be protective against the development of BPD.
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