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Inhibition of macrophage proinflammatory cytokine expression by steroids and recombinant IL-10

Y H Li1, A Brauner, B Jonsson

  • 1Neonatal Unit, Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden.

Biology of the Neonate
|August 18, 2001
PubMed

Insights

Steroids and recombinant IL-10 (rIL-10) reduce key inflammatory cytokines in chronic lung disease (CLD) models. This may explain how steroids benefit premature infants and suggests rIL-10 as a potential anti-inflammatory therapy.

Area of Science:

  • Neonatal respiratory medicine
  • Immunology
  • Pharmacology

Background:

  • Chronic lung disease (CLD) of prematurity involves prolonged respiratory failure in premature infants.
  • Proinflammatory cytokines are implicated in CLD development.
  • Steroids offer some clinical benefit in neonates with CLD.

Purpose of the Study:

  • To evaluate the downregulation of proinflammatory cytokines by dexamethasone, budesonide, and recombinant IL-10 (rIL-10).
  • To elucidate the mechanism behind the clinical benefits of steroids in infants with CLD.

Main Methods:

  • Utilized the THP-1 cell line stimulated with lipopolysaccharide and Ureaplasma urealyticum antigen.
  • Tested effects on macrophages from infant tracheobronchial aspirate fluid.
  • Examined rat alveolar macrophage cell lines.

Main Results:

  • Dexamethasone, budesonide, and human rIL-10 significantly inhibited IL-6 and TNF-alpha production in stimulated THP-1 cells and infant macrophages.
  • Steroids reduced IL-6 and TNF-alpha in rat macrophages, but rat rIL-10 did not show significant inhibition.
  • Human rIL-10 demonstrated anti-inflammatory effects.

Conclusions:

  • Steroids and human rIL-10 effectively downregulate proinflammatory cytokine production.
  • This mechanism likely explains the beneficial effects of steroids in CLD.
  • Recombinant IL-10 warrants consideration as an anti-inflammatory agent for high-risk neonates.

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