Original Research ARTICLE
Relationship between the Quorum network (Sensing/Quenching) and Clinical Features of Pneumonia and Bacteraemia caused by A. baumannii
- 1Investigación en Microbiología, Instituto de Investigación Biomedica de A Coruña Hospital Teresa Herrera, Spain
- 2Instituto de Biomedicina de Sevilla (IBIS), Spain
- 3Enfermedades Infecciosas y Sistema Inmune, Instituto de Biomedicina de Sevilla (IBIS), Spain
- 4Hospital Universitario Reina Sofía, Spain
- 5Instituto Salud Global Barcelona (ISGlobal), Spain
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 and mortality. 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 24h). 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.
Keywords: Quorum, Sensing/Quenching, Pneumonia, bacteraemia, Mortality, Acinetobacter
Received: 22 Sep 2018;
Accepted: 30 Nov 2018.
Edited by:Maria Soledad Ramirez, California State University, Fullerton, United States
Reviewed by:Vishvanath Tiwari, Central University of Rajasthan, India
Adriana S. Limansky, CONICET Instituto de Biología Molecular y Celular de Rosario (IBR), Argentina
Copyright: © 2018 Fernandez-Garcia, Ambroa, Blasco, Bleriot, LOPEZ, Cuenca, Alvarez-Marin, Martinez-Martinez, Vila, Rodríguez-Baño, Garnacho-Montero, Cisneros, Pascual, Pachon, Bou, Smani and Tomas. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Maria Tomas, Investigación en Microbiología, Instituto de Investigación Biomedica de A Coruña Hospital Teresa Herrera, A Coruña, Spain, firstname.lastname@example.org