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Updated: Aug 10, 2026
Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
Published on: March 18, 2014
Therapeutic Potential of Ginkgolic Acid C17:1 in Modulating PTEN/mtDNA/TLR9 Axis for Alleviating Chronic Pseudomonas
Shuke Rao1, Huiyan Jiang2, Jieyi Huang3
1Department of Pulmonary and Critical Care Medicine, Binhaiwan Central Hospital of Dongguan, Dongguan, Guangdong 523900, China.
Background:
Pseudomonas aeruginosa (PA) colonization drives persistent infection and inflammation in bronchiectasis, a condition lacking targeted biotherapies. Phosphatase and tensin homolog (PTEN) is a key regulator of immune homeostasis, and its plant-derived activator, Ginkgolic acid C17:1 (GAC 17:1), has emerged as a potential biotechnological therapeutic agent due to its anti-inflammatory properties.
Objectives:
This study aimed to investigate the therapeutic potential of GAC 17:1, a natural compound, in alleviating PA-induced airway injury by targeting the PTEN/mtDNA/TLR9 axis, thereby evaluating its role as a novel biotechnological intervention for immune modulation in bronchiectasis.
Materials And Methods:
A rat model of chronic PA-induced bronchial injury was established and divided into four groups: Control, PA-infected, PA-infected + GAC 17:1 (PTEN activator, 2 mg.kg-1), and PA-infected + SF1670 (PTEN inhibitor, 1.5 mg.kg-1). Lung pathology, function (FEV0.3, FVC, PEF), PTEN/TLR9/NF-κB expression (RT-qPCR, Western blot), mtDNA content, cytokine levels (IL-6, IL-17, TGF-β; ELISA), and Th17/Treg cell proportions (flow cytometry) were assessed.
Results:
PA infection downregulated PTEN, elevated mtDNA/TLR9/NF-κB, increased IL-6/IL-17 and Th17 cells, reduced TGF-β and Tregs, and impaired lung function. Treatment with GAC 17:1, the plant-derived PTEN activator, effectively restored PTEN expression, suppressed mtDNA release and TLR9/NF-κB signaling, rebalanced Th17/Treg immunity, reduced inflammatory cytokines, and significantly improved pulmonary function. Conversely, PTEN inhibition worsened all parameters.
Conclusions:
This study demonstrates that GAC 17:1, a natural bioactive compound, exerts potent significant effects in PA-related bronchiectasis by activating PTEN and inhibiting the mtDNA/TLR9/NF-κB pathway. Our findings highlight GAC 17:1 as a promising biotechnological candidate for developing plant-derived immunomodulatory therapies against chronic airway infections.
Insights
Ginkgolic acid C17:1 (GAC 17:1) activates PTEN to combat Pseudomonas aeruginosa-induced inflammation in bronchiectasis. This plant-derived compound shows promise as a novel therapy for chronic airway infections.
Area of Science:
- Immunology
- Pharmacology
- Biotechnology
Background:
- Pseudomonas aeruginosa (PA) colonization causes persistent inflammation in bronchiectasis, a condition lacking effective treatments.
- Phosphatase and tensin homolog (PTEN) regulates immune homeostasis; its activator, Ginkgolic acid C17:1 (GAC 17:1), possesses anti-inflammatory properties.
- GAC 17:1 is explored as a potential biotechnological therapeutic agent for immune modulation.
Purpose of the Study:
- To investigate the therapeutic potential of GAC 17:1 in mitigating PA-induced airway injury.
- To evaluate GAC 17:1's role in targeting the PTEN/mtDNA/TLR9 axis for immune modulation in bronchiectasis.
- To assess GAC 17:1 as a novel biotechnological intervention.
Main Methods:
- A rat model of chronic PA-induced bronchial injury was utilized.
- Groups included control, PA-infected, PA-infected + GAC 17:1, and PA-infected + PTEN inhibitor (SF1670).
- Assessed lung pathology, function, PTEN/TLR9/NF-κB expression, mtDNA content, cytokine levels, and Th17/Treg cell proportions.
Main Results:
- PA infection led to decreased PTEN, increased inflammatory markers (mtDNA/TLR9/NF-κB, IL-6, IL-17, Th17 cells), and impaired lung function.
- GAC 17:1 treatment restored PTEN, suppressed inflammation, rebalanced immune cells, and improved lung function.
- PTEN inhibition exacerbated the negative effects of PA infection.
Conclusions:
- GAC 17:1 effectively treats PA-related bronchiectasis by activating PTEN and inhibiting the mtDNA/TLR9/NF-κB pathway.
- This study highlights GAC 17:1 as a promising plant-derived immunomodulatory therapy candidate.
- GAC 17:1 represents a novel biotechnological approach for chronic airway infections.
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