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Harvesting Murine Alveolar Macrophages and Evaluating Cellular Activation Induced by Polyanhydride Nanoparticles
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Polymyxin B prevents lipopolysaccharide-induced release of tumor necrosis factor-alpha from alveolar macrophages

D C Stokes1, J L Shenep, M Fishman

  • 1Cardiopulmonary Division, St. Jude Children's Research Hospital, Memphis, TN 38101-0318.

The Journal of Infectious Diseases
|July 1, 1989
PubMed

Insights

Polymyxin B effectively blocks toxic lipopolysaccharide effects by inhibiting tumor necrosis factor-alpha (TNF-alpha) production in macrophages. This mechanism explains Polymyxin B

Area of Science:

  • Immunology
  • Pharmacology

Background:

  • Lipopolysaccharide (LPS) triggers toxic effects mediated by inflammatory cytokines.
  • The precise mechanisms by which Polymyxin B (PmB) counteracts LPS toxicity are not fully elucidated.

Purpose of the Study:

  • To investigate the effect of Polymyxin B on tumor necrosis factor-alpha (TNF-alpha) production by macrophages.
  • To elucidate the role of TNF-alpha inhibition in the protective effects of PmB against LPS.

Main Methods:

  • In vitro studies using isolated rat alveolar macrophages stimulated with LPS.
  • In vivo studies using a rat model with intratracheal LPS administration.
  • Assessment of TNF-alpha production in response to LPS and PmB treatment.

Main Results:

  • Polymyxin B significantly inhibited TNF-alpha production in both in vitro and in vivo models.
  • Gentamicin, an alternative antibiotic, enhanced TNF-alpha production at high concentrations.
  • PmB demonstrated inhibitory effects across a range of concentrations (100, 10, and 1 µg/ml).

Conclusions:

  • Polymyxin B inhibits LPS-induced TNF-alpha production.
  • Inhibition of TNF-alpha is a key mechanism explaining PmB's protective effects against LPS toxicity.

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