Pneumonia infection in mice reveals the involvement of the <i>feoA</i> gene in the pathogenesis of <i>Acinetobacter baumannii</i>

<i>Acinetobacter baumannii</i> has emerged in the last decade as an important nosocomial pathogen. To identify genes involved in the course of a pneumonia infection, gene expression profiles were obtained from <i>A. baumannii</i> ATCC 17978 grown in mouse infected lungs and in culture medium. Gene expression analysis allowed us to determine a gene, the A1S_0242 gene (<i>feoA</i>), over-expressed during the pneumonia infection. In the present work, we evaluate the role of this gene, involved in iron uptake. The inactivation of the A1S_0242 gene resulted in an increase susceptibility to oxidative stress and a decrease in biofilm formation, in adherence to A549 cells and in fitness. In addition, infection of <i>G. mellonella</i> and pneumonia in mice showed that the virulence of the Δ0242 mutant was significantly attenuated. Data presented in this work indicated that the A1S_0242 gene from <i>A. baumannii</i> ATCC 17978 strain plays a role in fitness, adhesion, biofilm formation, growth, and, definitively, in virulence. Taken together, these observations show the implication of the <i>feoA</i> gene plays in the pathogenesis of <i>A. baumannii</i> and highlight its value as a potential therapeutic target.