Invasive Acinetobacter baumannii ABC141 strain relies on the twin-arginine translocation (Tat) export system for adhesion to host cells
Acinetobacter baumannii is associated with severe hospital-acquired multi-drug resistant infections worldwide, causing significant mortality and morbidity in intensive care patients or under prolonged hospitalization. Multiple studies have recently shown that a proportion of circulating clinical isolates establish a transient multiplication niche inside phagocytic and non-phagocytic eukaryotic cells. We have previously demonstrated that the A. baumannii ABC141 strain invades human endothelial and epithelial cells, where it efficiently multiplies without induction of cytotoxicity. Here, we show that ABC141 adhesion, invasion, and intracellular multiplication depend on the growth stage, being most efficient in the exponential growth phase. To define the gene expression signature most favorable to an intracellular lifestyle, a transcriptomic comparison was carried out between exponentially grown ABC141 and cultures at the stationary phase. Although most of the pathways identified reflected growth-related metabolic changes, we observed an upregulation of the twin-arginine translocation (Tat) export system. Analysis of a mutant strain lacking the tatABC operon revealed this secretion system is only required for adhesion to host cells but not invasion and intracellular multiplication. These data highlight a new role for the Tat export pathway in A. baumannii pathogenesis. Overall design: Transcriptomic analysis using RNA-seq of Acinetobacter baumannii ABC141 grown in LB medium at 37°C. Two conditions were sampled: 15h of growth (OD600 2.2-2.5) and OD600 of 0.5.