Correlates of Elevated Interleukin-6 and 8-Hydroxy-2'-Deoxyguanosine Levels in Tracheal Aspirates from Very Low Birth Weight Infants Who Develop Bronchopulmonary Dysplasia.

Pediatr Neonatol

Department of Pediatrics, Changhua Christian Children's Hospital, Changhua City, Taiwan; School of Medicine, Kaohsiung Medical University, Kaohsiung City, Taiwan; School of Medicine, Chung Shan Medical University, Taichung City, Taiwan. Electronic address:

Published: February 2017

Background: Bronchopulmonary dysplasia (BPD) remains the most common complication of very low birth weight (VLBW) preterm infants, and inflammatory regulation plays a role in the development of the BPD. Interleukin-6 (IL-6) has an important role in airway inflammation and therefore can be used as a marker of airway injury. The study aimed to compare the changes between IL-6 and oxidative stress marker with 8-hydroxy-2'-deoxyguanosine (8-OHdG) from serum and tracheal aspiration (TA) in VLBW preterm infants following development of BPD.

Methods: This birth cohort study enrolled 80 VLBW preterm infants, including 26 who developed BPD. All infants completed the study and survived at 36 weeks postmenstrual age. IL-6 and 8-OHdG concentrations from serum and TA on Day 1 and Day 28 after birth were measured using immunoassay.

Results: IL-6 and 8-OHdG in serum and TA were higher in the BPD group than in the non-BPD group on the 1 day after birth (p < 0.05). The IL-6 and 8-OHdG levels in TA fluid were persistently increased on the 28 day of life in the BPD group (p < 0.05). The TA IL-6 was positively correlated with 8-OHdG levels on the 1 day (r = 0.64, p < 0.05) and 28 day of life (r = 0.76, p < 0.05). Based on receiver operating characteristic curves as a predictor of BPD development, TA IL-6 (cutoff, 456.8 pg/mg) had 81.5% sensitivity and 77.8% specificity, whereas TA 8-OHdG (cutoff, 4.4 ng/mg) had a sensitivity of 81.5% and a specificity of 64.4%.

Conclusion: Persistent inflammation with oxidative DNA damage in the respiratory tract may be a crucial mechanism in BPD.

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http://dx.doi.org/10.1016/j.pedneo.2016.01.004DOI Listing

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