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Updated: Jun 13, 2026
The Utilization of Oropharyngeal Intratracheal PAMP Administration and Bronchoalveolar Lavage to Evaluate the Host Immune Response in Mice
Published on: April 2, 2014
Comparison of the effect of LPS and PAM3 on ventilated lungs
Hans P Hauber1, Dörte Karp, Torsten Goldmann
1Pathophysiology of Inflammation, Research Center Borstel, Borstel, Germany. hphauber@fz-borstel.de
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.
Insights
Lipopeptide PAM3 from Gram-positive bacteria, like LPS, enhances ventilator-induced lung inflammation. PAM3 also increases pulmonary resistance in mechanically ventilated mice, unlike LPS.
Area of Science:
- Pulmonary inflammation research
- Microbiology and immunology
- Mechanical ventilation studies
Background:
- Lipopolysaccharide (LPS) from Gram-negative bacteria is known to worsen lung inflammation during mechanical ventilation.
- The impact of Gram-positive bacterial components on ventilated lungs remains largely uncharacterized.
Purpose of the Study:
- To investigate the effects of lipopolysaccharide (LPS) and a lipopeptide (PAM3) from Gram-positive bacteria on mechanically ventilated lungs.
- To compare the inflammatory and functional responses induced by LPS and PAM3 in a mouse model.
Main Methods:
- Mechanical ventilation was applied to C57/Bl6 mice.
- Intratracheal administration of sterile saline (sham), LPS (1-5 microg), and PAM3 (50-200 nM).
- Measurement of lung function (resistance, compliance), inflammatory markers (MIP-2, TNFalpha mRNA), and neutrophil influx.
Main Results:
- Mechanical ventilation alone increased resistance and decreased compliance.
- PAM3 significantly increased pulmonary resistance, whereas LPS did not.
- Both LPS and PAM3 elevated MIP-2 and TNFalpha mRNA expression.
- Neutrophil influx was significantly increased by both LPS (at 5 microg) and PAM3 (at both concentrations).
Conclusions:
- PAM3, similar to LPS, exacerbates ventilator-induced lung inflammation.
- PAM3 uniquely increases pulmonary resistance in ventilated lungs, distinguishing it from LPS.
- Further research is needed to elucidate the role of lipopeptides in ventilator-associated lung injury (VALI).
