Matrix porosity is associated with biofilm survival during prosthetic joint infection.

Biofilms are a cause of chronic, non-healing infections. is a proficient biofilm forming pathogen commonly isolated from prosthetic joint infections that develop following primary arthroplasty. Extracellular adhesion protein (Eap), previously characterized in planktonic or non-biofilm populations as being an adhesin and immune evasion factor, was recently identified in the exoproteome of biofilms. This work demonstrates that Eap and its two functionally orphaned homologs EapH1 and EapH2, contribute to biofilm structure and prevent macrophage invasion and phagocytosis into these communities. Biofilms unable to express Eap proteins demonstrated increased porosity and reduced biomass. We describe a role for Eap proteins using a mouse model of prosthetic joint infection. Results suggest that the protection conferred to biofilms by Eap proteins is a function of biofilm structural stability that interferes with the leukocyte response to biofilm-associated bacteria.