ArticleInfection and immunity2016
Enhanced Clearance of Pseudomonas aeruginosa by Peroxisome Proliferator-Activated Receptor Gamma.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Insights into the activity, production, and signaling circuits of homoserine lactones in mammalian cells.iScience · 2026Article
- Multifaceted Antipathogenic Activity of Two Novel Natural Products, Chermesiterpenoid B and Chermesiterpenoid B Seco Acid Methyl Ester, Against Pseudomonas aeruginosa.Microbial biotechnology · 2025Article
- Article
- HowInternational journal of molecular sciences · 2023Review
- Pioglitazone Modifies Kupffer Cell Function and Protects againstInternational journal of molecular sciences · 2022Article
- Use of oral anti-diabetic drugs and risk of hospital and intensive care unit admissions for infections.The American journal of the medical sciences · 2022Article
- The PPAR-γ agonist pioglitazone exerts proinflammatory effects in bronchial epithelial cells during acute Pseudomonas aeruginosa pneumonia.Clinical and experimental immunology · 2022Article
- Pathogenesis of thePathogens (Basel, Switzerland) · 2022Review
- The Effect of PGC-1alpha-SIRT3 Pathway Activation onPathogens (Basel, Switzerland) · 2022Article
- Repurposing of substances with lactone moiety for the treatment of γ-Hydroxybutyric acid and γ-Butyrolactone intoxication through modulating paraoxonase and PPARγ.Frontiers in pharmacology · 2022Article
- Post-treatment with the PPAR-γ agonist pioglitazone inhibits inflammation and bacterial growth during Klebsiella pneumonia.Respiratory research · 2021Article
- Long non-coding RNA LINC00488 facilitates thyroid cancer cell progression through miR-376a-3p/PON2.Bioscience reports · 2021Article
- The Relevance of Noncoding DNA Variations of Paraoxonase Gene Cluster in Atherosclerosis-Related Diseases.International journal of molecular sciences · 2021Review
- Erythropoietin Promotes Infection Resolution and Lowers Antibiotic Requirements inFrontiers in immunology · 2021Article
- UPR modulation of host immunity by Pseudomonas aeruginosa in cystic fibrosis.Clinical science (London, England : 1979) · 2020Article
- Pseudomonas aeruginosa Induced Host Epithelial Cell Mitochondrial Dysfunction.Scientific reports · 2019Article
- Macrophages exposed to HIV viral protein disrupt lung epithelial cell integrity and mitochondrial bioenergetics via exosomal microRNA shuttling.Cell death & disease · 2019Article
- Immunometabolism at the interface between macrophages and pathogens.Nature reviews. Immunology · 2019Review
- Macrophage nuclear receptors: Emerging key players in infectious diseases.PLoS pathogens · 2019Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The pathogenic profile of Pseudomonas aeruginosa is related to its ability to secrete a variety of virulence factors. Quorum sensing (QS) is a mechanism wherein small diffusible molecules, specifically acyl-homoserine lactones, are produced by P. aeruginosa to promote virulence. We show here that macrophage clearance of P. aeruginosa (PAO1) is enhanced by activation of the nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPARγ). Macrophages treated with a PPARγ agonist (pioglitazone) showed enhanced phagocytosis and bacterial killing of PAO1. It is known that PAO1 QS molecules are inactivated by PON-2. QS molecules are also known to inhibit activation of PPARγ by competitively binding PPARγ receptors. In accord with this observation, we found that infection of macrophages with PAO1 inhibited expression of PPARγ and PON-2. Mechanistically, we show that PPARγ induces macrophage paraoxonase 2 (PON-2), an enzyme that degrades QS molecules produced by P. aeruginosa Gene silencing studies confirmed that enhanced clearance of PAO1 in macrophages by PPARγ is PON-2 dependent. Further, we show that PPARγ agonists also enhance clearance of P. aeruginosa from lungs of mice infected with PAO1. Together, these data demonstrate that P. aeruginosa impairs the ability of host cells to mount an immune response by inhibiting PPARγ through secretion of QS molecules. These studies define a novel mechanism by which PPARγ contributes to the host immunoprotective effects during bacterial infection and suggest a role for PPARγ immunotherapy for P. aeruginosa infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.