AUTHOR=Fernandez-Garcia Laura , Ambroa Antón , Blasco Lucia , Bleriot Ines , López Maria , Alvarez-Marin Rocio , Fernández-Cuenca Felipe , Martinez-Martinez Luis , Vila Jordi , Rodríguez-Baño Jesús , Garnacho-Montero Jose , Cisneros Jose Miguel , Pascual Alvaro , Pachón Jeronimo , Bou German , Smani Younes , Tomás Maria 

TITLE=Relationship Between the Quorum Network (Sensing/Quenching) and Clinical Features of Pneumonia and Bacteraemia Caused by A. baumannii

JOURNAL=Frontiers in Microbiology

VOLUME=9

YEAR=2018

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2018.03105

DOI=10.3389/fmicb.2018.03105

ISSN=1664-302X

ABSTRACT=<p><italic>Acinetobacter baumannii</italic> (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 <italic>A. baumannii</italic> isolated in the “II Spanish Study of <italic>A. baumannii</italic> GEIH-REIPI 2000-2010” (<italic>Genbank Umbrella Bioproject</italic> PRJNA422585), a multicentre study describing the relationship between the Quorum network in <italic>A. baumannii</italic> and the development of pneumonia and associated bacteraemia. Expression of the <italic>aidA</italic> gene (encoding the AidA protein, QQ enzyme) was lower (<italic>P</italic> &lt; 0.001) in strains of <italic>A. baumannii</italic> isolated from patients with bacteraemic pneumonia than in strains isolated from patients with non-bacteraemic pneumonia. Moreover, <italic>aidA</italic> 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 H<sub>2</sub>O<sub>2</sub> (inhibitor of AidA protein, QS activation). However, in the <italic>A. baumannii</italic> strains isolated from patients with non-bacteraemic pneumonia, <italic>aidA</italic> gene expression was regulated by stressors such as 3-oxo-C12-HSL and H<sub>2</sub>O<sub>2</sub>. In an <italic>in vivo Galleria mellonella</italic> model of <italic>A. baumannii</italic> infection, the <italic>A. baumannii</italic> ATCC 17978 strain was associated with higher mortality (100% at 24 h) than the mutant, <italic>abaI</italic>-deficient, strain (carrying a synthetase enzyme of Acyl homoserine lactone molecules) (70% at 24 h). These data suggest that the QS (<italic>abaR</italic> and <italic>abaI</italic> genes)/QQ (<italic>aidA</italic> gene) network affects the development of secondary bacteraemia in pneumonia patients and also the virulence of <italic>A. baumannii</italic>.</p>