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Interleukin 6 receptor alpha expression in PMNs isolated from prematurely born neonates: decreased expression is

Robert A Campbell1, Mark J Cody2, Bhanu K Manne1

  • 1Program in Molecular Medicine, University of Utah, Salt Lake City, UT, USA.

Pediatric Research
|April 10, 2019
PubMed

Insights

Neonatal neutrophils have reduced mammalian target of rapamycin (mTOR) signaling, leading to lower interleukin-6 receptor alpha (IL-6Rα) synthesis. This impaired IL-6Rα production may prolong inflammation and increase illness in preterm infants.

Area of Science:

  • Immunology
  • Neonatal Medicine
  • Molecular Biology

Background:

  • Dysregulated inflammation in neonates contributes to significant morbidity and mortality.
  • Neutrophil-mediated inflammation is a key driver of inflammatory tissue damage.
  • The mammalian target of rapamycin (mTOR) pathway regulates IL-6 receptor alpha (IL-6Rα) expression in neutrophils.

Purpose of the Study:

  • To investigate the hypothesis that preterm neonatal neutrophils fail to synthesize IL-6Rα due to alterations in mTOR signaling.
  • To compare IL-6Rα expression and mTOR signaling in neutrophils from preterm neonates and healthy adults.

Main Methods:

  • Studied IL-6Rα and PAF receptor expression, and mTOR signaling in plasma and neutrophils from neonates and adults.
  • Utilized techniques including ELISA, RT-PCR, western blotting, flow cytometry, and immunocytochemistry.

Main Results:

  • Neonatal plasma had less soluble IL-6Rα than adult plasma.
  • While IL-6Rα mRNA levels were similar, IL-6Rα protein expression was decreased in preterm neonatal neutrophils.
  • mTOR signaling was reduced in preterm neonatal neutrophils following PAF stimulation.

Conclusions:

  • Preterm neonatal neutrophils show diminished mTOR signaling, resulting in reduced IL-6Rα synthesis.
  • This decreased IL-6Rα synthesis may impair IL-6/IL-6Rα trans-signaling, potentially leading to prolonged inflammation and increased morbidity in preterm infants.
Abstract

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