Griffith Thao, Tell Dina, Green Stefan J, Ford Ashley, Bohan Adam, Grunwaldt Jennifer, Amin Sachin, White-Traut Rosemary, Janusek Linda
Author Affiliations: Department of Family and Community Health Nursing, Marcella Niehoff School of Nursing, Loyola University Chicago, Maywood, Illinois (Drs Griffith, and Tell, Mrs Ford, and Dr Janusek); Department of Internal Medicine, Division of Infectious Disease, Rush University, Chicago, Illinois (Dr Green); Division of Neonatology, Loyola University Medical Center, Maywood, Illinois (Mr Bohan, Mrs Grunwaldt, and Dr Amin); Nursing Research, Children's Wisconsin, Milwaukee, Wisconsin (Dr White-Traut); and Women, Children and Family Health Science, College of Nursing, University of Illinois at Chicago, Chicago, Illinois (Dr White-Traut).
Adv Neonatal Care. 2025 Feb 1;25(1):6-17. doi: 10.1097/ANC.0000000000001208. Epub 2024 Dec 26.
Early life stress exposure in preterm infants may alter DNA methylation of NR3C1 and HSD11B2 , disrupting neurobehaviors needed for oral feeding (PO) skill development.
To (1) examine the feasibility of the study protocol; (2) describe early life stress, DNA methylation of NR3C1 and HSD11B2 , and PO skill development; and (3) explore the association between DNA methylation of NR3C1 and HSD11B2 and infant characteristics, early life stress, and PO skill development.
We employed a longitudinal descriptive pilot study (N = 10). Infant characteristics were collected from the infant's electronic medical record. Early life stress was assessed via the modified Neonatal Infant Stressor Scale. DNA methylation of NR3C1 exon 1F and HSD11B2 promoter regions was analyzed from the infant's buccal samples. PO skill development was evaluated using the Early Feeding Skills Assessment.
Infants who experienced more acute and chronic stress during their neonatal intensive care unit hospitalization demonstrated higher DNA methylation at CpG 17 and 31 of the NR3C1 exon 1F and at CpG 4 and 28 of the HSD11B2 promoter regions. Infants with higher DNA methylation at these CpG sites also exhibited less optimal PO skill development and experienced longer transition from first to full PO.
Our findings revealed relationships among early life stress, DNA methylation of NR3C1 and HSD11B2 , and PO skill development in preterm infants. Future research is warranted to examine the multiomics pathways whereby early life stress influences the phenotypes of infant outcomes.
早产儿早期生活应激暴露可能会改变NR3C1和HSD11B2的DNA甲基化，破坏经口喂养（PO）技能发展所需的神经行为。
（1）检验研究方案的可行性；（2）描述早期生活应激、NR3C1和HSD11B2的DNA甲基化以及PO技能发展情况；（3）探讨NR3C1和HSD11B2的DNA甲基化与婴儿特征、早期生活应激及PO技能发展之间的关联。
我们采用了一项纵向描述性试点研究（N = 10）。从婴儿的电子病历中收集婴儿特征。通过改良的新生儿应激源量表评估早期生活应激。从婴儿的颊部样本中分析NR3C1外显子1F和HSD11B2启动子区域的DNA甲基化。使用早期喂养技能评估来评价PO技能发展情况。
在新生儿重症监护病房住院期间经历更多急性和慢性应激的婴儿，在NR3C1外显子1F的CpG 17和31以及HSD11B2启动子区域的CpG 4和28处显示出更高的DNA甲基化。在这些CpG位点具有较高DNA甲基化的婴儿，其PO技能发展也不太理想，并且从首次经口喂养到完全经口喂养的过渡时间更长。
我们的研究结果揭示了早产儿早期生活应激、NR3C1和HSD11B2的DNA甲基化以及PO技能发展之间的关系。未来有必要进行研究，以检验早期生活应激影响婴儿结局表型的多组学途径。
