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Activation of macrophage nuclear factor-kappa B and induction of inducible nitric oxide synthase by LPS

Ying-Hua Li1, Zhong-Qun Yan, Annelie Brauner

  • 1Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden. Ying-Hau.Li@kbh.ki.se

Respiratory Research
|September 27, 2002
PubMed

Insights

Lipopolysaccharide (LPS) stimulates nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in macrophages. Steroids like dexamethasone and budesonide reduce these inflammatory responses, potentially explaining their benefit in chronic lung disease.

Area of Science:

  • Neonatal immunology
  • Pulmonary medicine
  • Inflammation research

Background:

  • Chronic lung disease (CLD) of prematurity is a significant neonatal care challenge.
  • Bacterial infections and inflammation are implicated in CLD development.
  • Steroids offer some therapeutic benefit in neonates with CLD.

Purpose of the Study:

  • To investigate lipopolysaccharide (LPS)-induced nitric oxide (NO) production, inducible nitric oxide synthase (iNOS) expression, and nuclear factor-kappaB (NF-kappaB) activation in rat alveolar macrophages.
  • To evaluate the effects of dexamethasone and budesonide on these LPS-induced responses in vitro.

Main Methods:

  • Nitrite levels were measured using the Griess reaction.
  • iNOS expression was assessed via Western blot and RT-PCR.
  • NF-kappaB activation was analyzed using electrophoretic mobility shift assay (EMSA).

Main Results:

  • LPS dose-dependently stimulated NO production in macrophages, an effect enhanced by IFN-gamma.
  • Budesonide and dexamethasone significantly attenuated LPS-induced NO production and iNOS expression (mRNA and protein).
  • LPS exposure triggered NF-kappaB activation, correlating with iNOS expression.

Conclusions:

  • Gram-negative bacterial infection and associated inflammation are key factors in CLD pathogenesis.
  • Steroids may benefit neonates with CLD by down-regulating iNOS expression and NO production.
  • These findings elucidate a potential mechanism for steroid efficacy in neonatal lung disease.
Abstract

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