The trimeric autotransporter adhesin Ata controls key virulence traits of .

is a Gram-negative pathogen that causes a multitude of nosocomial infections. The trimeric autotransporter adhesin (Ata) belongs to the superfamily of trimeric autotransporter adhesins which are important virulence factors in many Gram-negative species. Phylogenetic profiling revealed that is present in 78% of all sequenced isolates but only in 2% of the closely related species and . Employing a markerless deletion mutant of ATCC 19606 we show that adhesion to and invasion into human endothelial and epithelial cells depend on Ata. Infection of primary human umbilical cord vein endothelial cells (HUVECs) with led to the secretion of interleukin (IL)-6 and IL-8 in a time- and Ata-dependent manner. Furthermore, infection of HUVECs by WT was associated with higher rates of apoptosis via activation of caspases-3 and caspase-7, but not necrosis, in comparison to ∆. Ata deletion mutants were furthermore attenuated in their ability to kill larvae of and to survive in larvae when injected at sublethal doses. This indicates that Ata is an important multifunctional virulence factor in that mediates adhesion and invasion, induces apoptosis and contributes to pathogenicity .