High tissue factor in lungs and plasma associates with respiratory morbidity in preterm infants

Anniina Palojärvi1, Sture Andersson, Sanna Siitonen

  • 1Children's Hospital, Helsinki University Hospital, Helsinki, Finland. anniina.palojarvi@gmail.com

Insights

In preterm infants, high levels of tissue factor (TF) in the lungs and plasma are linked to respiratory distress syndrome (RDS). Interleukin-6 and Interleukin-8 may drive TF upregulation, contributing to infant lung injury.

Area of Science:

  • Neonatal Medicine
  • Pulmonology
  • Immunology

Background:

  • Respiratory distress syndrome (RDS) in preterm infants involves inflammation and intra-alveolar fibrin formation.
  • Tissue factor (TF) acts as a critical link between inflammatory processes and coagulation cascades.
  • Understanding TF's role in neonatal inflammation is crucial for managing preterm infant respiratory complications.

Purpose of the Study:

  • To investigate the relationship between tissue factor (TF) and cytokines in preterm infants.
  • To elucidate the role of TF in the inflammatory response associated with respiratory distress syndrome (RDS).
  • To explore potential mechanisms of TF upregulation in sick neonates.

Main Methods:

  • Measurement of TF in plasma and tracheal aspirates from 56 preterm infants (600-1500 g birthweight).
  • Analysis of TF expression on monocytes via flow cytometry.
  • Quantification of 13 plasma cytokines during the first week of life.

Main Results:

  • Plasma TF levels increased, peaking on day 3, and correlated with RDS severity and inversely with paO2/FIO2.
  • Tracheal aspirate TF was significantly higher than plasma TF on day 1 and correlated with plasma TF.
  • Plasma TF correlated with pro-inflammatory cytokines IL-8 and IL-6, but not IL-1 or TNF-α.

Conclusions:

  • Elevated TF in the lungs and plasma is associated with respiratory morbidity in preterm infants.
  • Upregulation of TF in sick newborns may be mediated by IL-6 and IL-8.
  • High TF and pro-inflammatory cytokines likely contribute to pulmonary and extrapulmonary injury in preterm infants via inflammatory pathways.
Abstract

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