Neonatology | 2021
Commentary on the Truncated Splice Variant of the GM-CSF Receptor Beta-Chain in Peripheral Blood Serves as Severity Biomarker of Respiratory Failure in Newborns
Abstract
In this issue, Schulte et al. [1] report novel data demonstrating increased expression of GM-CSFR (IT) mRNA in peripheral blood cells of newborn infants with respiratory illness compared to those without respiratory signs and symptoms. Since GM-CSFR (IT) is a truncated receptor isoform that inhibits GM-CSF signaling in monocytes and macrophages, its expression may inhibit cellular processes dependent upon GM-CSF, including pulmonary surfactant catabolism and innate host defense in the lung. Increased levels of the inhibitory GM-CSF receptor fragment provide potential mechanisms to inhibit surfactant catabolism, thereby enhancing surfactant pools as an adaptive response to respiratory illness in neonates. The findings serve to highlight some of the complex cellular and molecular mechanisms controlling surfactant homeostasis in the neonatal lung.