Staphylococcal enterotoxin C2 promotes
osteogenesis of mesenchymal stem cells
and accelerates fracture healing
As one of the heat-stable enterotoxins, Staphylococcal enterotoxin C2 (SEC2) is synthesized
by Staphylococcus aureus, which has been proved to inhibit the growth of tumour cells, and
is used as an antitumour agent in cancer immunotherapy. Although SEC2 has been reported
to promote osteogenic differentiation of human mesenchymal stem cells (MSCs), the in vivo
function of SCE2 in animal model remains elusive. The aim of this study was to further elucidate
the in vivo effect of SCE2 on fracture healing.
Materials and Methods
Rat MSCs were used to test the effects of SEC2 on their proliferation and osteogenic differentiation
potentials. A rat femoral fracture model was used to examine the effect of local
administration of SEC2 on fracture healing using radiographic analyses, micro-CT analyses,
biomechanical testing, and histological analyses.
While SEC2 was found to have no effect on rat MSCs proliferation, it promoted the osteoblast
differentiation of rat MSCs. In the rat femoral fracture model, the local administration of
SEC2 accelerated fracture healing by increasing fracture callus volumes, bone volume over
total volume (BV/TV), and biomechanical recovery. The SEC2 treatment group has superior
histological appearance compared with the control group.
These data suggest that local administration of SEC2 may be a novel therapeutic approach
to enhancing bone repair such as fracture healing.
Cite this article: Bone Joint Res 2018;7:179–186.