Staphylococcus aureus are gram-positive bacteria that cause skin and soft tissue infections. The continual incidence of infection is of great concern especially with the advent of methicillin resistant S. aureus (MRSA). Continued investigation on mechanisms our body uses to fight bacterial infection is vital. Our study suggests that the body takes advantage of a mechanism that mineralizes type-I collagen of bone and tendon to also mineralize bacteria. Serum driven bacterial mineralization may be a mechanism of innate immunity to control bacterial infection by affecting their viability or growth.

S. aureus was incubated in serum under various experimental conditions to determine the necessary factors in the mechanism of mineralization, as well as the extent and location of formed mineral. These experiments indicate that: (1) A large serum nucleator is required to generate mineral crystals (2) TNAP is essential for mineralization by activating the serum nucleator. Inhibition of TNAP prevents bacterial mineralization and addition of pure TNAP restores the ability of serum to mineralize bacteria. (3) Fetuin is necessary for localizing mineralization within the interior of the bacteria. Without fetuin, mineral forms predominantly outside bacteria. These results demonstrate a similar mechanism of mineralization as type-I collagen (4) In addition, previous studies have demonstrated that bacteria have similar size exclusion properties as collagen[1,2,3]. Small molecules (< 14kDa) can penetrate the bacterial matrix while molecules (>50 kDa) are excluded [4,5,6]. Lastly, through TEM it is observed that the mineral is formed throughout bacteria and has a similar morphology to hydroxyapatite.