On the opposite, in the UTI model, the impairment of the interaction of ElrA with FHL2 led to a systemic infection but with intermediate E. faecalis burdens in mice organs compared to wild-type strain (higher counts) and the fully deleted elrA strain (lower counts), revealing that ElrA contributes to virulence in ascending urinary tract infection. This evidence concerns the gene FHL2 and bacterial urinary tract infection.