Relationship Between the Quorum Network (Sensing/Quenching) and Clinical Features of Pneumonia and Bacteraemia Caused by A. baumannii
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Updated: Jan 31, 2026

Anti-virulent Disruption of Pathogenic Biofilms using Engineered Quorum-quenching Lactonases
Published on: January 1, 2016
Laura Fernandez-Garcia1, Antón Ambroa1, Lucia Blasco1
1Microbiology Department-Biomedical Research Institute A Coruña (INIBIC), Hospital A Coruña (CHUAC), University of A Coruña (UDC), A Coruña, Spain.
Abstract:
Acinetobacter baumannii (Ab) is one of the most important pathogens associated with nosocomial infections, especially pneumonia. Interest in the Quorum network, i.e., Quorum Sensing (QS)/Quorum Quenching (QQ), in this pathogen has grown in recent years. The Quorum network plays an important role in regulating diverse virulence factors such as surface motility and bacterial competition through the type VI secretion system (T6SS), which is associated with bacterial invasiveness. In the present study, we investigated 30 clinical strains of A. baumannii isolated in the "II Spanish Study of A. baumannii GEIH-REIPI 2000-2010" (Genbank Umbrella Bioproject PRJNA422585), a multicentre study describing the relationship between the Quorum network in A. baumannii and the development of pneumonia and associated bacteraemia. Expression of the aidA gene (encoding the AidA protein, QQ enzyme) was lower (P < 0.001) in strains of A. baumannii isolated from patients with bacteraemic pneumonia than in strains isolated from patients with non-bacteraemic pneumonia. Moreover, aidA expression in the first type of strain was not regulated in the presence of environmental stress factors such as the 3-oxo-C12-HSL molecule (substrate of AidA protein, QQ activation) or H2O2 (inhibitor of AidA protein, QS activation). However, in the A. baumannii strains isolated from patients with non-bacteraemic pneumonia, aidA gene expression was regulated by stressors such as 3-oxo-C12-HSL and H2O2. In an in vivo Galleria mellonella model of A. baumannii infection, the A. baumannii ATCC 17978 strain was associated with higher mortality (100% at 24 h) than the mutant, abaI-deficient, strain (carrying a synthetase enzyme of Acyl homoserine lactone molecules) (70% at 24 h). These data suggest that the QS (abaR and abaI genes)/QQ (aidA gene) network affects the development of secondary bacteraemia in pneumonia patients and also the virulence of A. baumannii.
Insights
Acinetobacter baumannii quorum sensing and quenching network impacts pneumonia virulence and secondary bloodstream infections. Lower aidA gene expression in bacteraemic pneumonia suggests altered Quorum Sensing/Quenching regulation.
Area of Science:
- Microbiology
- Infectious Diseases
- Molecular Biology
Background:
- Acinetobacter baumannii is a major cause of hospital-acquired infections, particularly pneumonia.
- The Quorum Sensing (QS) and Quorum Quenching (QQ) network regulates virulence factors in A. baumannii.
- Understanding the QS/QQ network's role in pneumonia and bacteraemia is crucial for infection control.
Purpose of the Study:
- To investigate the relationship between the Quorum network in A. baumannii and the development of pneumonia and bacteraemia.
- To analyze the expression of the aidA gene (QQ enzyme) in clinical strains under different conditions.
- To evaluate the virulence of A. baumannii strains in an in vivo model.
Main Methods:
- Analysis of 30 clinical A. baumannii strains from a multicentre study.
- Measurement of aidA gene expression in response to environmental stressors (3-oxo-C12-HSL, H2O2).
- In vivo virulence testing using the Galleria mellonella infection model with wild-type and abaI-deficient strains.
Main Results:
- Lower aidA gene expression was observed in strains from patients with bacteraemic pneumonia compared to non-bacteraemic pneumonia.
- aidA expression in bacteraemic pneumonia strains was not regulated by 3-oxo-C12-HSL or H2O2, unlike non-bacteraemic strains.
- The abaI-deficient mutant showed reduced mortality in Galleria mellonella compared to the wild-type strain.
Conclusions:
- The QS/QQ network, involving abaR, abaI, and aidA genes, influences the development of secondary bacteraemia in pneumonia.
- Alterations in QS/QQ regulation are associated with increased virulence of A. baumannii.
- Targeting the QS/QQ network may offer novel therapeutic strategies against A. baumannii infections.
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