Bacteria inhibit biosynthesis of bone matrix proteins in human osteoblasts.
The effect of extracts from Staphylococcus aureus and Staphylococcus epidermidis on bone matrix production were assessed by analyzing the biosynthesis of osteocalcin and Type I collagen in a human osteoblastic osteosarcoma cell line (MG-63). In MG-63 cells, extracts from Staphylococcus aureus and Staphylococcus epidermidis decreased 1,25(OH)2-vitamin D3 stimulated osteocalcin biosynthesis, and insulin-like growth factor I induced production of Type I collagen in a concentration dependent manner. The basal rate of osteocalcin and Type I collagen formation was unaffected by the bacterial extracts. The inhibitory effect of the bacteria on osteocalcin biosynthesis was seen after 24 hours of treatment and was maintained for at least 96 hours. The extracts of Staphylococcus aureus and Staphylococcus epidermidis enhanced prostaglandin E2 formation in the MG-63 cells. Abolition of the prostaglandin E2 response by treatment with indomethacin and flurbiprofen did not affect bacteria induced inhibition of osteocalcin production. Stimulation of osteocalcin biosynthesis by 1,25(OH)2-vitamin D3 was associated with a decreased rate of cell proliferation. The inhibitory action of the bacterial extracts was not linked to any inhibition of [3H]-thymidine incorporation into deoxyribonucleic acid. These data show that extracts of Staphylococcus aureus and Staphylococcus epidermidis have the ability to inhibit the biosynthesis of bone matrix proteins by a nonprostaglandin and noncytotoxic dependent mechanism and suggest that bone loss in inflammatory processes containing Staphylococcus aureus or Staphylococcus epidermidis may not be caused only by enhanced bone resorption but also by decreased bone formation.
Lerner
U H
UH
Department of Oral Cell Biology, University of Umeå, Sweden.
Sundqvist
G
G
Ohlin
A
A
Rosenquist
J B
JB
D002117:Calcitriol / Q000494:pharmacology; D002455:Cell Division; D003094:Collagen / Q000378:metabolism*; D015232:Dinoprostone / Q000378:metabolism; D005480:Flurbiprofen / Q000494:pharmacology; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology; D010006:Osteoblasts / Q000187:drug effects / Q000378:metabolism* / Q000382:microbiology*; D015675:Osteocalcin / Q000378:metabolism*; D013211:Staphylococcus aureus; D013212:Staphylococcus epidermidis; D014407:Tumor Cells, Cultured
D015675:Osteocalcin; D005480:Flurbiprofen; D007334:Insulin-Like Growth Factor I; D003094:Collagen; D002117:Calcitriol; D015232:Dinoprostone; D007213:Indomethacin