EFFECT OF STAPHYLO CO CCAL PEPTID O GLYCAN ON OSTEO CL AST DIFFERENTIATION_Chinese Journal of Reparative and Reconstructive Surgery

Authors：

RENLirong ¹ ,  XUYongqing ² , WANGHai ² , HEXiaoqing ² , SONGMuguo ² , CHENXueqiu ¹

1. Kunming Medical University, Kunming Yunnan, 650504, P. R. China;
2. Department of Orthopedics, Kunming General Hospital of Chengdu Military Region;

Corresponding author：

XUYongqing, Email: xuyongqingkm@163.net

Keywords：

Staphylococcal peptidoglycan; Osteoclast; Differentiation; Bone resorption

DOI：

10.7507/1002-1892.20160203

Video：

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Objective To investigate the effect of Staphylococcal peptidoglycan (PGN-sa) on raw264.7 cells differentiating into osteoclasts. Methods There were 5 groups in the experiment: 100 ng/mL PGN-sa group, 200 ng/mL PGN-sa group, 400 ng/mL PGN-sa group, positive control group [100 ng/mL receptor activator of nuclear factor κB ligand (RANKL)], and blank control group (PBS). Raw264.7 cells were cultured with different concentrations of PGN-sa, RANKL, or PBS for 5 days, and then tartrate resistant acid phosphatase (TRAP) staining was used to detect the formation of osteoclast-like cells; Image-Pro Plus 6.0 software was used to detect the bone resorption areas of osteoclast-like cells; and MTT assay was used to observe the proliferation activity of raw264.7 cells. Results TRAP staining showed that PGN-sa and RANKL can induce raw264.7 cells to differentiate into osteoclast-like cells; different concentrations of PGNsa groups had more osteoclast-like cells formation than blank control group (P < 0.05), and the number of osteoclast-like cells significantly increased with the increase of PGN-sa concentrations (P < 0.05). Bone resorption cavity experiment showed that bone resorption cavities were obvious in different concentrations of PGN-sa groups and in positive control group, and the area of bone absorption cavities was increased with the increasing PGN-sa concentrations, showing significant difference between groups (P < 0.05). MTT assay showed that no significant difference was found in the absorbance (A) value between different concentrations of PGN-sa groups and blank control group, and between different concentrations of PGN-sa groups (P > 0.05). Conclusion PGN-sa can promote raw264.7 cells to differentiate into osteoclasts with bone resorption activity.

Citation： RENLirong, XUYongqing, WANGHai, HEXiaoqing, SONGMuguo, CHENXueqiu. EFFECT OF STAPHYLO CO CCAL PEPTID O GLYCAN ON OSTEO CL AST DIFFERENTIATION. Chinese Journal of Reparative and Reconstructive Surgery, 2016, 30(8): 1006-1010. doi: 10.7507/1002-1892.20160203 Copy

1.	Montanaro L, Testoni F, Poggi A, et al. Emerging pathogenetic mechanisms of the implant-related osteomyelitis by Staphylococcus aureus. Int J Artif Organs, 2011, 34(9):781-788.
2.	Liu ZQ, Deng GM, Foster S, et al. Staphylococcal peptidoglycans induce arthritis. Arthritis Res, 2001, 3(6):375-380.
3.	Park OJ, Yang J, Kim J, et al. Enterococcus faecalis attenuates the differentiation of macrophages into osteoclasts. J Endod, 2015, 41(5): 658-662.
4.	黄金亮, 唐辉, 徐永清.骨髓炎流行病学.国际骨科学杂志, 2011, 32(2):94-95.
5.	Tuchscherr L, Kreis CA, Hoerr V, et al. Staphylococcus aureus develops increased resistance to antibiotics by forming dynamic small colony variants during chronic osteomyelitis. J Antimicrob Chemother, 2016, 71(2):438-448.
6.	Kalinka J, Hachmeister M, Geraci J, et al. Staphylococcus aureus isolates from chronic osteomyelitis are characterized by high host cell invasion and intracellular adaptation, but still induce inflammation. Int J Med Microbiol, 2014, 304(8):1038-1049.
7.	Wang H, He XQ, Jin T, et al. Wnt11 plays an important role in the osteogenesis of human mesenchymal stem cells in a PHA/FN/ALG composite scaffold:possible treatment for infected bone defect. Stem Cell Res Ther, 2016, 7:18.
8.	Jin T, Zhu YL, Li J, et al. Staphylococcal protein A, Panton-Valentine leukocidin and coagulase aggravate the bone loss and bone destruction in osteomyelitis. Cell Physiol Biochem, 2013, 32(2):322-333.
9.	Josse J, Velard F, Gangloff SC. Staphylococcus aureus vs. osteoblast: relationship and consequences in osteomyelitis. Front Cell Infect Microbiol, 2015, 5:85.
10.	Zecconi A, Scali F. Staphylococcus aureus virulence factors in evasion from innate immune defenses in human and animal diseases. Immunol Lett, 2013, 150(1-2):12-22.
11.	Kishimoto T, Kaneko T, Ukai T, et al. Peptidoglycan and lipopolysaccharide synergistically enhance bone resorption and osteoclastogenesis. J Periodontal Res, 2012, 47(4):446-454.
12.	Kim J, Yang J, Park OJ, et al. Lipoproteins are an important bacterial component responsible for bone destruction through the induction of osteoclast differentiation and activation. J Bone Miner Res, 2013, 28(11):2381-2391.
13.	Takami M, Kim N, Rho J, et al. Stimulation by toll-like receptors inhibits osteoclast differentiation. J Immunol, 2002, 169(3):1516-1523.
14.	Kobayashi K, Takahashi N, Jimi E, et al. Tumor necrosis factor alpha stimulates osteoclast differentiation by a mechanism independent of the ODF/RANKL-RANK interaction. J Exp Med, 2000, 191(2):275-286.
15.	Zhou C, Liu W, He W, et al. Saikosaponin a inhibits RANKLinduced osteoclastogenesis by suppressing NF-κB and MAPK pathways. Int Immunopharmacol, 2015, 25(1):49-54.
16.	Yao W, Li K, Liao K. Macropinocytosis contributes to the macrophage foam cell formation in RAW264.7 cells. Acta Biochim Biophys Sin (Shanghai), 2009, 41(9):773-780.
17.	Hsu H, Lacey DL, Dunstan CR, et al. Tumor necrosis factor receptor family member rank mediates osteoclast differentiation and activation induced by osteoprotegerin ligand. Proc Natl Acad Sci U S A, 1999, 96(7):3540-3545.
18.	Adamopoulos IE, Mellins ED. Alternative pathways of osteoclastogenesis in inflammatory arthritis. Nat Rev Rheumatol, 2015, 11(3):189-194.
19.	Trouillet-Assant S, Gallet M, Nauroy P, et al. Dual impact of live Staphylococcus aureus on the osteoclast lineage, leading to increased bone resorption. J Infect Dis, 2015, 211(4):571-581.
20.	Lau YS, Wang W, Sabokbar A, et al. Staphylococcus aureus capsular material promotes osteoclast formation. Injury, 2006, 37 Suppl 2: S41-48.

1. Montanaro L, Testoni F, Poggi A, et al. Emerging pathogenetic mechanisms of the implant-related osteomyelitis by Staphylococcus aureus. Int J Artif Organs, 2011, 34(9):781-788.
2. Liu ZQ, Deng GM, Foster S, et al. Staphylococcal peptidoglycans induce arthritis. Arthritis Res, 2001, 3(6):375-380.
3. Park OJ, Yang J, Kim J, et al. Enterococcus faecalis attenuates the differentiation of macrophages into osteoclasts. J Endod, 2015, 41(5): 658-662.
4. 黄金亮, 唐辉, 徐永清.骨髓炎流行病学.国际骨科学杂志, 2011, 32(2):94-95.
5. Tuchscherr L, Kreis CA, Hoerr V, et al. Staphylococcus aureus develops increased resistance to antibiotics by forming dynamic small colony variants during chronic osteomyelitis. J Antimicrob Chemother, 2016, 71(2):438-448.
6. Kalinka J, Hachmeister M, Geraci J, et al. Staphylococcus aureus isolates from chronic osteomyelitis are characterized by high host cell invasion and intracellular adaptation, but still induce inflammation. Int J Med Microbiol, 2014, 304(8):1038-1049.
7. Wang H, He XQ, Jin T, et al. Wnt11 plays an important role in the osteogenesis of human mesenchymal stem cells in a PHA/FN/ALG composite scaffold:possible treatment for infected bone defect. Stem Cell Res Ther, 2016, 7:18.
8. Jin T, Zhu YL, Li J, et al. Staphylococcal protein A, Panton-Valentine leukocidin and coagulase aggravate the bone loss and bone destruction in osteomyelitis. Cell Physiol Biochem, 2013, 32(2):322-333.
9. Josse J, Velard F, Gangloff SC. Staphylococcus aureus vs. osteoblast: relationship and consequences in osteomyelitis. Front Cell Infect Microbiol, 2015, 5:85.
10. Zecconi A, Scali F. Staphylococcus aureus virulence factors in evasion from innate immune defenses in human and animal diseases. Immunol Lett, 2013, 150(1-2):12-22.
11. Kishimoto T, Kaneko T, Ukai T, et al. Peptidoglycan and lipopolysaccharide synergistically enhance bone resorption and osteoclastogenesis. J Periodontal Res, 2012, 47(4):446-454.
12. Kim J, Yang J, Park OJ, et al. Lipoproteins are an important bacterial component responsible for bone destruction through the induction of osteoclast differentiation and activation. J Bone Miner Res, 2013, 28(11):2381-2391.
13. Takami M, Kim N, Rho J, et al. Stimulation by toll-like receptors inhibits osteoclast differentiation. J Immunol, 2002, 169(3):1516-1523.
14. Kobayashi K, Takahashi N, Jimi E, et al. Tumor necrosis factor alpha stimulates osteoclast differentiation by a mechanism independent of the ODF/RANKL-RANK interaction. J Exp Med, 2000, 191(2):275-286.
15. Zhou C, Liu W, He W, et al. Saikosaponin a inhibits RANKLinduced osteoclastogenesis by suppressing NF-κB and MAPK pathways. Int Immunopharmacol, 2015, 25(1):49-54.
16. Yao W, Li K, Liao K. Macropinocytosis contributes to the macrophage foam cell formation in RAW264.7 cells. Acta Biochim Biophys Sin (Shanghai), 2009, 41(9):773-780.
17. Hsu H, Lacey DL, Dunstan CR, et al. Tumor necrosis factor receptor family member rank mediates osteoclast differentiation and activation induced by osteoprotegerin ligand. Proc Natl Acad Sci U S A, 1999, 96(7):3540-3545.
18. Adamopoulos IE, Mellins ED. Alternative pathways of osteoclastogenesis in inflammatory arthritis. Nat Rev Rheumatol, 2015, 11(3):189-194.
19. Trouillet-Assant S, Gallet M, Nauroy P, et al. Dual impact of live Staphylococcus aureus on the osteoclast lineage, leading to increased bone resorption. J Infect Dis, 2015, 211(4):571-581.
20. Lau YS, Wang W, Sabokbar A, et al. Staphylococcus aureus capsular material promotes osteoclast formation. Injury, 2006, 37 Suppl 2: S41-48.

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Chinese Journal of Reparative and Reconstructive Surgery

EFFECT OF STAPHYLO CO CCAL PEPTID O GLYCAN ON OSTEO CL AST DIFFERENTIATION

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