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Ace is an adhesin to collagen from  Enterococcus faecalis  expressed conditionally after growth in serum or in the presence of collagen. Here, we generated an  ace  deletion mutant and showed that it was significantly attenuated versus wild-type OG1RF in a mixed infection rat endocarditis model ( P <0.0001), while no differences were observed in a peritonitis model. Complemented OG1RFΔ ace  (pAT392:: ace ) enhanced early (4 h) heart valve colonization versus OG1RFΔ ace  (pAT392) ( P  = 0.0418), suggesting that Ace expression is important for early attachment. By flow cytometry using specific anti-recombinant Ace (rAce) immunoglobulins (Igs), we showed  in vivo  expression of Ace by OG1RF cells obtained directly from infected vegetations, consistent with our previous finding of anti-Ace antibodies in  E. faecalis  endocarditis patient sera. Finally, rats actively immunized against rAce were less susceptible to infection by OG1RF than non-immunized ( P  = 0.0004) or sham-immunized ( P  = 0.0475) by CFU counts. Similarly, animals given specific anti-rAce Igs were less likely to develop  E. faecalis  endocarditis ( P  = 0.0001) and showed fewer CFU in vegetations ( P  = 0.0146). In conclusion, we have shown for the first time that Ace is involved in pathogenesis of, and is useful for protection against,  E. faecalis  experimental endocarditis.

Importance of the Collagen Adhesin Ace in Pathogenesis and Protection against Enterococcus faecalis Experimental Endocarditis