Airway expression of the epithelial sodium channel α-subunit correlates with cortisol in term newborns.
cross_sectional · Level IV
Where this comes from
- Record sourced from PubMed, PMID 21768316.
- Also identified by DOI 10.1542/peds.2011-0167.
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Abstract
Glucocorticoids have profound effects on lung maturation and function. In in vitro and animal models, they induce epithelial sodium channels (ENaCs) in the airway epithelium, a process that is important to perinatal lung fluid clearance. The objective of this study was to determine whether, in newborn infants, airway ENaC expression is associated with cortisol concentrations. Cord blood, saliva, and cells from nasal epithelium were obtained from 69 infants delivered at term. Epithelial and saliva sampling was repeated 3 times: <3, 22 to 29, and 40 to 54 hours postnatally. Cortisol, thyrotropin, and free triiodothyronine concentrations were measured with immunoassays, and expression of α-ENaC and β-ENaC was quantified with real-time reverse-transcriptase polymerase chain reaction. Expression of α-ENaC <30 minutes postnatally correlated with cord plasma cortisol in infants delivered by elective cesarean delivery. In addition, in the total study population <2 hours postnatally, α-ENaC expression correlated with salivary cortisol concentrations. β-ENaC expression, in contrast, showed no association with cortisol concentrations. A significant decrease in β-ENaC expression during the first postnatal day was revealed, whereas timing of the peak in α-ENaC expression seemed to depend on mode of delivery. These results support a role in humans for endogenous glucocorticoids in the regulation of airway ion transport. This finding may be a physiologic mechanism mediating pulmonary adaptation in the newborn infant.
Medical subject headings
- Epithelial Sodium Channels
- Gene Expression Regulation, Developmental
- Hydrocortisone
- Nasal Mucosa