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| Research progress of osteoarticular involvement with brucellosis |
| LIANG Chen1, WEI Wei2, LIANG Xiu-wen1, DE En-jin1, WANG Li-jun1 |
1. Hulunbeier People’s Hospital of, Hulunbuir 021008, China;
2. Hulunbeier Center for Disease Control and Prevention, Hulunbuir 021008, China |
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Abstract Osteoarticular brucellosis is the most common presentation of human disease in the world. There are three most common forms of osteoarticular involvement are peripheral arthritis, sacroiliitis, and spondylitis. Brucella abortus induces bone damage through diverse mechanisms in which TNF-a and RANKL modulator of bone homeostasis are involved. These processes are driven by inflammatory cells, like macrophages, neutrophils, Th17 CD4C T, and T cells. These bacteria inhibit bone matrix deposition by osteoblasts and modify the phenotype of those cells to produce matrix metalloproteinases (MMPs) and cytokine secretion, contributing to bone matrix degradation. Finally, the molecular mechanisms of osteoarticular brucellosis discovered that how the interaction between B. abortus and osteoarticular cells may play an important role in producing damage in joint and bone.
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Received: 30 March 2018
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Fund:Supported by the National Key Clinical Specialty Construction Project (No. 2011-470), the Inner Mongolia Autonomous Region Science and Technology Major Projects (No. 2060901), and the Hulunbuir Science and Technology Major Projects (No.2014-812)
Liang Chen and Wei Wei contributed equally to the article. |
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Corresponding Authors:
De en-jin, Email: hlbesdej@163.com
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[1] Scian R, Barrionuevo P, Rodriguez AM, et al. Brucella abortus invasion of synoviocytes inhibits apoptosis and induces bone resorption through RANKL expression[J]. Infect Immun, 2013,81(6):1940-1951. DOI: 10.1128/IAI.01366-12
[2] Giambartolomei GH, Arriola Benitez PC, Delpino MV. Brucella and osteoarticular cell activation: partners in crime[J]. Front Microbiol, 2017, 20(8):256. DOI:10.3389/fmicb.2017.00256
[3] Scian R, Barrionuevo P, Fossati CA, et al. Brucella abortus invasion of osteoblasts inhibits bone formation[J]. Infect Immun, 2012, 80(7):2333-2345. DOI:10.1128/IAI.00208-12
[4] Giambartolomei GH, Scian R, Acosta-Rodríguez E, et al. Brucella abortus-infected macrophages modulate T lymphocytes to promote osteoclastogenesis via IL-17[J]. Am J Pathol, 2012, 181(3):887-896. DOI:10.1016/j.ajpath.2012.05.029
[5] Chakraborty S, Kloos B, Harre U, et al. Pasteurella multocida toxin triggers RANKL-independent osteoclastogenesis[J]. Front Immunol, 2017,27(8):185. DOI:10.3389/fimmu.2017.00185
[6] Souza PP, Lerner UH. The role of cytokines in inflammatory bone loss[J]. Immunol Invest, 2013, 42(7):555-622. DOI:10.3109/08820139.2013.822766
[7] Prideaux M, Staines KA, Jones ER, et al. MMP and TIMP temporal gene expression during osteocytogenesis[J]. Gene Expr Patterns, 2015,18(1/2):29-36. DOI:10.1016/j.gep.2015.04.004
[8] Liu KG, He QH, Tan JW, et al. Expression of TNF-α, VEGF, and MMP-3 mRNAs in synovial tissues and their roles in fibroblast-mediated osteogenesis in ankylosing spondylitis[J]. Genet Mol Res, 2015,14(2):6852-6858. DOI:10.4238/2015.June.18.28
[9] Goenka R, Parent MA, ElzerPH. B cell-deficient mice display markedly enhanced resistance to the intracellular bacterium Brucella abortus[J]. J Infect Dis, 2011,203(8):1136-1146. DOI:10.1093/infdis/jiq171
[10] García Samartino C, Delpino MV, Pott GodoyC, et al. Brucella abortus induces the secretion of proinflammatory mediators from glial cells leading toastrocyte apoptosis[J]. Am J Pathol, 2010,176(3):1323-1338. DOI:10.2353/ajpath.2010.090503
[11] Goenka R, Guirnalda PD, Black SJ, et al. B Lymphocytes provide an infection niche for intracellular bacterium Brucella abortus[J]. J Infect Dis, 2012, 206(1):91-98. DOI:10.1093/infdis/jis310
[12] Ikeda K, Takeshita S. The role of osteoclast differentiation and function in skeletal homeostasis[J]. J Biochem, 2016, 159(1):1-8. DOI:10.1093/jb/mvv112
[13] Horowitz MC, Fretz JA, Lorenzo JA. How B cells influence bone biology in health and disease[J]. Bone, 2010, 47(3):472-479. DOI:10.1016/j.bone.2010.06.011
[14] Prideaux M, Findlay DM, Atkins GJ. Osteocytes: the master cells in bone remodelling[J]. Curr Opin Pharmacol, 2016, 28, 24-30. DOI:10.1016/j.coph.2016.02.003
[15] Galli C, Passeri G, Macaluso GM. Osteocytes and WNT: the mechanical control of bone formation[J]. J Dent Res, 2010, 89(4):331-343. DOI:10.1177/0022034510363963
[16] Alotaibi MK, Kitase Y, Shuler CF. Smad2 overexpression induces alveolar bone loss and up regulates TNF-α, and RANKL[J]. Arch Oral Biol, 2016, 71:38-45. DOI:10.1016/j.archoralbio.2016.06.023
[17] D’Amelio P, Grimaldi A, Bernabei P, et al. Immune system and bone metabolism: Does thymectomy influence postmenopausal bone loss in humans[J]. Bone, 2006, 39(3):658-665. DOI:10.1016/j.bone.2006.03.009
[18] Scian R, Barrionuevo P, Fossati CA, et al. Brucella abortus invasion of osteoblasts Inhibits bone formation[J]. Infect Immun, 2012, 80(7):2333-2345. DOI:10.1128/IAI.00208-12
[19] Sabokbar A, Mahoney DJ, Hemingway F, et al. Non-canonical (RANKL-Independent) pathways of osteoclast differentiation and their role in musculoskeletal diseases[J]. Clin Rev Allergy Immunol, 2016,51(1):16-26. DOI:10.1007/s12016-015-8523-6
[20] Komori T.Cell death in chondrocytes, osteoblasts, and osteocytes[J].Int J Mol Sci, 2016,17(12): E2045. DOI:10.3390/ijms17122045
[21] Scian R, Barrionuevo P, Giambartolomei GH, et al. Potential role of fibroblast-like synoviocytes in joint damage induced by Brucella abortus infection through production and induction of matrix metalloproteinases[J]. Infect Immun, 2011, 79(9):3619-3632. DOI:10.1128/IAI.05408-11
[22] Franco MP, Mulder M, Gilman RH. Human brucellosis[J]. Lancet Infect Dis 2007, 7(12): 775-786. |
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2018, Vol. 34 
