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An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
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Activation of T cells in preterm infants with respiratory distress syndrome

Riikka Turunen1, Outi Vaarala, Irmeli Nupponen

  • 1Department of Pediatrics, Kanta-Hame Central Hospital, Hameenlinna, Finland. riikka.s.turunen@helsinki.fi

Neonatology
|May 27, 2009
PubMed

Insights

In preterm infants, respiratory distress syndrome (RDS) is linked to lower T cell counts and increased T cell activation. This activation may predict the development of bronchopulmonary dysplasia (BPD).

Area of Science:

  • Neonatal immunology
  • Respiratory medicine
  • Inflammatory diseases

Background:

  • Preterm infants with respiratory distress syndrome (RDS) exhibit systemic inflammation.
  • The role of lymphocytes in RDS and their potential contribution to bronchopulmonary dysplasia (BPD) require further investigation.

Purpose of the Study:

  • To determine if T cells are activated in preterm infants diagnosed with RDS.
  • To assess the association between T cell activation and the subsequent development of BPD.

Main Methods:

  • Compared 34 preterm infants with RDS to 21 without RDS.
  • Utilized flow cytometry to analyze CD4 and CD8 cell counts and expression of CD54 and CD62L on postnatal days 1, 3, and 7.
  • Defined T cell activation by increased CD54 expression and decreased CD62L expression.

Main Results:

  • Infants with RDS had lower CD4 and CD8 cell counts on day 3 (p=0.02).
  • RDS was associated with increased CD4+CD54+ cells (p=0.001-0.03) and decreased CD8+CD62L+ cells (p=0.02) on days 1 and 3.
  • Higher CD54 expression on T cells in infants with RDS predicted BPD development.

Conclusions:

  • RDS in preterm infants is characterized by reduced T cell counts and heightened T cell activation.
  • Elevated T cell activation serves as a predictor for BPD development.
  • Systemic T cell activation may play a role in mediating inflammation and the pathogenesis of BPD.
Abstract

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