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Preterm infants have deficient monocyte and lymphocyte cytokine responses to group B streptococcus

Andrew J Currie1, Samantha Curtis, Tobias Strunk

  • 1School of Veterinary & Biomedical Sciences, Murdoch University, Murdoch, Western Australia. a.currie@murdoch.edu.au

Infection and Immunity
|February 9, 2011
PubMed

Insights

Preterm infants show impaired immune responses to Group B Streptococcus (GBS), with deficient cytokine production from monocytes and lymphocytes, increasing their susceptibility to GBS infections.

Area of Science:

  • Neonatal immunology
  • Infectious disease
  • Streptococcal infections

Background:

  • Group B Streptococcus (GBS) is a major cause of neonatal sepsis, particularly in preterm infants.
  • The immunological responses of preterm infants to GBS are not well understood, despite their increased susceptibility and poorer outcomes.
  • Understanding these responses is crucial for developing targeted interventions.

Purpose of the Study:

  • To compare the immune cell cytokine responses to GBS in preterm infants, term infants, and healthy adults.
  • To investigate the cell source and kinetics of cytokine production and GBS phagocytosis.
  • To identify specific immune defects contributing to GBS susceptibility in preterm neonates.

Main Methods:

  • Mononuclear cell and whole-blood cytokine assays were performed using heat-killed GBS (HKGBS).
  • Quantification of HKGBS phagocytosis by immune cells.
  • Comparison of responses across preterm infants (GA 26–33 weeks), term infants, and adults; some experiments included live GBS and complement supplementation.

Main Results:

  • Preterm infants exhibited significantly impaired secretion of tumor necrosis factor (TNF) and interleukin-6 (IL-6) in response to HKGBS compared to term infants and adults.
  • Cytokine production was primarily monocytic and linked to phagocytosis; very preterm infants (<30 weeks GA) had fewer cytokine-producing monocytes.
  • Lymphocyte-associated cytokine responses were deficient in both preterm and term infants compared to adults, indicating broader neonatal immune limitations.

Conclusions:

  • A subset of preterm monocytes demonstrates a non-responsive phenotype to GBS, contributing to increased infection risk.
  • Generalized weaker lymphocyte responses in newborns further compound the susceptibility of preterm infants to GBS.
  • These findings highlight critical immune deficits in preterm neonates that predispose them to severe GBS infections.

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