Inflammatory mediators of stress exposure and neurodevelopment in very preterm infants: Protocol for the stress neuro‐immune study

• Published in: Journal of advanced nursing Vol. 75; no. 10; pp. 2236 - 2245
• Main Authors: Nist, Marliese Dion, Pickler, Rita H., Steward, Deborah K., Harrison, Tondi M., Shoben, Abigail B.
• Format: Journal Article
• Language: English
• Published: England Wiley Subscription Services, Inc 01.10.2019
• Subjects: Baby foods; Blood; Child development; Child Development - physiology; Cortisol; cytokines; Female; Hair; Humans; Infant, Newborn; Infant, Premature - growth & development; Infants; Inflammation; Inflammation Mediators - physiology; Intensive care; Male; Measurement; Neonatal care; neonatal intensive care; Neurobehavioral functioning; neurodevelopment; Neurology; Newborn babies; nursing; Premature babies; Premature birth; preterm infant; Process analysis; repeated measures; Stress; Stress, Physiological - physiology; Within-subjects design; United States > US; stress; neurodevelopment; inflammation; cytokines; nursing; preterm infant; neonatal intensive care; repeated measures
• ISSN: 0309-2402; 1365-2648; 1365-2648
• DOI: 10.1111/jan.14079

Aims (a) Determine relationships among stress exposure, inflammation, and neurodevelopment in very preterm infants and determine the mediated effect of inflammation on the relationship between stress exposure and neurodevelopment; (b) describe cytokine trajectories following birth and determine the effect of stress exposure on these trajectories; and (c) examine relationships between stress exposure and chronic stress responses in very preterm infants. Design Non‐experimental, repeated measures. Methods Very preterm infants born 28–31 weeks post menstrual age will be enrolled. Cumulative stress exposure over the first 14 days of life will be measured using the Neonatal Infant Stressor Scale. Blood will be collected weekly for the quantification of cytokines. Neurodevelopment will be assessed using the Neurobehavioral Assessment of the Preterm Infant and hair for quantification of hair cortisol will be collected at 35 weeks post menstrual age. Multiple linear regression and conditional process analysis will be used to analyse the relationships among stress exposure, inflammation and neurodevelopment. Linear mixed models will be used to determine inflammatory trajectories over time. IRB approval for the study was received May 2017, and funding from the National Institute of Nursing Research was awarded July 2017. Discussion This study will determine the extent to which inflammation mediates the relationship between stress exposure and neurodevelopment. Interventions to attenuate inflammation in preterm infants may improve outcomes. Impact Determining the potentially modifiable mediators of stress exposure and neurodevelopment in preterm infants is critical to improving long‐term outcomes. 目的 (a) 确定极早早产儿应激暴露、炎症和神经发育之间的关系,并确定炎症在应激暴露和神经发育之间关系中介导的作用;(b)描述出生后的细胞因子轨迹,并确定应激暴露对这些轨迹的影响; (c)研究极早早产儿的应激暴露与慢性应激反应之间的关系。设计非试验性、可重复的测量。方法将矫正胎龄为28至31周的极早早产儿作为测量对象。使用新生儿应激源量表测量出生后14天的累积应激暴露。每周收集血液用于定量细胞因子。通过早产婴儿的神经行为评估来评估神经发育,并且在矫正胎龄35周收集用于定量毛发皮质醇的毛发。采用多元线性回归和条件过程分析方法,分析应激暴露、炎症和神经发育之间的关系。线性混合模型将用于确定随时间推移的炎症轨迹。该项研究于2017年5月由IRB批准,并于2017年7月获得国立护理医学研究所的资助经费。讨论本研究将确定炎症可以在多大程度上调节应激暴露与神经发育之间的关系。减轻早产儿炎症的干预措施可能会改善预后。影响确定早产儿应激暴露和神经发育的潜在可调节介质对于改善长期预后至关重要。