Comparison of the effect of LPS and PAM3 on ventilated lungs

BMC Pulm Med. 2010 Apr 20:10:20. doi: 10.1186/1471-2466-10-20.

Abstract

Background: While lipopolysaccharide (LPS) from Gram-negative bacteria has been shown to augment inflammation in ventilated lungs information on the effect of Gram-positive bacteria is lacking. Therefore the effect of LPS and a lipopetide from Gram-positive bacteria, PAM3, on ventilated lungs were investigated.

Methods: C57/Bl6 mice were mechanically ventilated. Sterile saline (sham) and different concentrations of LPS (1 microg and 5 microg) and PAM3 (50 nM and 200 nM) were applied intratracheally. Lung function parameters and expression of MIP-2 and TNFalpha as well as influx of neutrophils were measured.

Results: Mechanical ventilation increased resistance and decreased compliance over time. PAM3 but not LPS significantly increased resistance compared to sham challenge (P < 0.05). Both LPS and PAM3 significantly increased MIP-2 and TNFalpha mRNA expression compared to sham challenge (P < 0.05). The numbers of neutrophils were significantly increased after LPS at a concentration of 5 microg compared to sham (P < 0.05). PAM3 significantly increased the numbers of neutrophils at both concentrations compared to sham (P < 0.05).

Conclusions: These data suggest that PAM3 similar to LPS enhances ventilator-induced inflammation. Moreover, PAM3 but not LPS increases pulmonary resistance in ventilated lungs. Further studies are warranted to define the role of lipopetides in ventilator-associated lung injury.

Publication types

  • Comparative Study

MeSH terms

  • Airway Resistance / drug effects
  • Airway Resistance / physiology
  • Animals
  • Chemokine CXCL2 / metabolism
  • Dose-Response Relationship, Drug
  • Gram-Negative Bacteria / metabolism*
  • Gram-Positive Bacteria / metabolism*
  • Lipopeptides / metabolism
  • Lipopeptides / pharmacology*
  • Lipopolysaccharides / metabolism
  • Lipopolysaccharides / pharmacology*
  • Lung / cytology
  • Lung / drug effects*
  • Lung / physiology
  • Lung Compliance / drug effects
  • Lung Compliance / physiology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Models, Animal
  • Neutrophils / cytology
  • Neutrophils / drug effects
  • Respiration, Artificial*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Chemokine CXCL2
  • Cxcl2 protein, mouse
  • Lipopeptides
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha