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Pseudomonas aeruginosa Induced Lung Injury Model
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Pseudomonas aeruginosa Induced Lung Injury Model

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Peroxisome proliferator-activated receptors mediate host cell proinflammatory responses to Pseudomonas aeruginosa

Aruna Jahoor1, Rashila Patel, Amanda Bryan

  • 1Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, 3601 4th St., Lubbock, TX 79430, USA.

Journal of Bacteriology
|January 8, 2008
PubMed

Insights

Pseudomonas aeruginosa uses 3-oxododecanoyl homoserine lactone (3OC(12)-HSL) to trigger inflammation. Researchers identified peroxisome proliferator-activated receptors (PPARs) as mammalian receptors for 3OC(12)-HSL, suggesting potential anti-inflammatory therapies.

Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Pseudomonas aeruginosa quorum sensing molecule 3OC(12)-HSL induces host inflammation.
  • The mechanism of 3OC(12)-HSL-mediated host response and its receptors remain unidentified.
  • 3OC(12)-HSL exacerbates disease during P. aeruginosa infections.

Purpose of the Study:

  • To identify mammalian receptors for 3OC(12)-HSL.
  • To elucidate the role of these receptors in 3OC(12)-HSL-induced inflammation.

Main Methods:

  • Examined nuclear hormone receptor expression in murine fibroblasts and human lung epithelial cells.
  • Assessed 3OC(12)-HSL's effect on PPARbeta/delta and PPARgamma transcriptional activity.
  • Investigated the impact of PPARgamma agonist rosiglitazone on 3OC(12)-HSL-induced inflammation.

Main Results:

  • Identified expression of PPARbeta/delta and PPARgamma in both cell types.
  • 3OC(12)-HSL activated PPARbeta/delta and inhibited PPARgamma activity.
  • Rosiglitazone blocked 3OC(12)-HSL's proinflammatory effects, indicating mutual antagonism at PPARgamma.

Conclusions:

  • PPARbeta/delta and PPARgamma are putative mammalian receptors for 3OC(12)-HSL.
  • PPARgamma agonists, like rosiglitazone, may serve as anti-inflammatory treatments for P. aeruginosa infections.

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