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Hospital acquired pneumonia with high-risk bacteria is associated with increased pulmonary matrix metalloproteinase

Bernhard Schaaf1, Cornelia Liebau, Volkhard Kurowski

  • 1Medical Clinic III, University of Lübeck, Lübeck, Germany. schaaf@uni-luebeck.de

BMC Pulmonary Medicine
|August 14, 2008
PubMed
Abstract

Insights

Hospital-acquired pneumonia (HAP) elevates pulmonary matrix metalloproteinases (MMP), particularly MMP-9. High-risk bacteria like S. aureus and Pseudomonas species significantly increase MMP levels and activity in HAP patients.

Area of Science:

  • Pulmonary Medicine
  • Microbiology
  • Biochemistry

Background:

  • Neutrophil-derived matrix metalloproteinases (MMP) play a role in bacterial defense but can also cause lung damage.
  • Matrix metalloproteinases (MMP) are elevated in the lungs during hospital-acquired pneumonia (HAP).
  • Bacterial virulence differs in HAP, with high-risk species like S. aureus and Pseudomonas implicated.

Purpose of the Study:

  • To investigate the impact of high-risk bacteria on pulmonary matrix metalloproteinase (MMP) concentrations in patients with hospital-acquired pneumonia (HAP).

Main Methods:

  • Analyzed MMP-8, MMP-9, and tissue inhibitors of metalloproteinases (TIMP) in bronchoalveolar lavage (BAL) fluid from 37 HAP patients and 16 controls using ELISA.
  • Assessed MMP-9 activity via zymography in BAL samples.

Main Results:

  • MMP-9 activity was significantly higher in HAP patients compared to controls (149 +/- 41 vs. 34 +/- 11, p < 0.0001).
  • Patients infected with high-risk bacteria exhibited markedly elevated MMP-9 concentrations (1168 +/- 266 ng/ml) and activity (325 +/- 106) compared to those with low-risk bacteria.
  • MMP-8 and MMP-9 levels correlated with mechanical ventilation status and C-reactive protein (CRP) levels.

Conclusions:

  • Pulmonary MMP concentrations and activity are elevated in HAP patients.
  • This elevation is most pronounced in HAP cases involving high-risk bacteria.
  • Mechanical ventilation may contribute to protease activation in HAP.

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