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本文引用的文献

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Resolution of Staphylococcus aureus biofilm infection using vaccination and antibiotic treatment.使用疫苗接种和抗生素治疗解决金黄色葡萄球菌生物膜感染。
Infect Immun. 2011 Apr;79(4):1797-803. doi: 10.1128/IAI.00451-10. Epub 2011 Jan 10.
2
Treating osteomyelitis: antibiotics and surgery.治疗骨髓炎:抗生素和手术。
Plast Reconstr Surg. 2011 Jan;127 Suppl 1:177S-187S. doi: 10.1097/PRS.0b013e3182001f0f.
3
Attachment of Staphylococcus aureus is required for activation of nuclear factor kappa B in human osteoblasts.金黄色葡萄球菌的黏附对于人成骨细胞中核因子 kappa B 的激活是必需的。
Acta Biochim Biophys Sin (Shanghai). 2010 Dec;42(12):883-92. doi: 10.1093/abbs/gmq096. Epub 2010 Nov 3.
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Molecular mechanism of NLRP3 inflammasome activation.NLRP3 炎性体激活的分子机制。
J Clin Immunol. 2010 Sep;30(5):628-31. doi: 10.1007/s10875-010-9440-3. Epub 2010 Jun 30.
5
[Contribution of sigma B to environmental stress tolerance in Listeria monocytogenes--a review].[西格玛B对单核细胞增生李斯特菌环境应激耐受性的贡献——综述]
Wei Sheng Wu Xue Bao. 2009 Oct;49(10):1282-8.
6
Osteomyelitis.骨髓炎
Dis Mon. 2010 Jan;56(1):5-31. doi: 10.1016/j.disamonth.2009.07.001.
7
Interaction of staphylococci with bone.葡萄球菌与骨的相互作用。
Int J Med Microbiol. 2010 Feb;300(2-3):193-204. doi: 10.1016/j.ijmm.2009.10.003. Epub 2009 Nov 3.
8
Staphylococcus aureus: new evidence for intracellular persistence.金黄色葡萄球菌:细胞内持续存在的新证据。
Trends Microbiol. 2009 Feb;17(2):59-65. doi: 10.1016/j.tim.2008.11.005. Epub 2009 Feb 7.
9
Nod1 and Nod2 in innate immunity and human inflammatory disorders.先天免疫及人类炎症性疾病中的Nod1和Nod2
Biochem Soc Trans. 2007 Dec;35(Pt 6):1479-84. doi: 10.1042/BST0351479.
10
Osteoblasts express NLRP3, a nucleotide-binding domain and leucine-rich repeat region containing receptor implicated in bacterially induced cell death.成骨细胞表达NLRP3,这是一种含有核苷酸结合域和富含亮氨酸重复序列的受体,与细菌诱导的细胞死亡有关。
J Bone Miner Res. 2008 Jan;23(1):30-40. doi: 10.1359/jbmr.071002.

金黄色葡萄球菌与成骨细胞的相互作用(综述)

Interaction of Staphylococcus aureus with osteoblasts (Review).

作者信息

Shi Sifeng, Zhang Xianlong

机构信息

Department of Orthopaedic Surgery, Shanghai Sixth People's Hospital, Jiao Tong University, Shanghai, P.R. China.

出版信息

Exp Ther Med. 2012 Mar;3(3):367-370. doi: 10.3892/etm.2011.423. Epub 2011 Dec 20.

DOI:10.3892/etm.2011.423
PMID:22969897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3438663/
Abstract

Orthopedic infection is refractory to cure. Staphylococcus aureus (S. aureus) is the main causative pathogen responsible for orthopedic infection. S. aureus is capable of not only colonizing bone matrix, but also invading osteoblasts, which may play a significant role in the persistence and recurrence of osteomyelitis. Internalization requires the involvement of cytoskeletal elements, including actin microfilaments, microtubules and clathrin-coated pits. Microfilaments are most significant in the invasion process. S. aureus is capable of remaining alive in osteoblasts for a long period of time. Decreased sensitivity to antibiotics capable of penetrating host cells increases the difficulties of eradicating S. aureus. Osteoblasts, invaded by S. aureus, play a significant role in the initiation and maintenance of inflammatory immune responses. These osteoblasts recruit leukocytes and phagocytes to the site of inflammation via the expression of cytokines. Apoptosis is observed in osteoblasts invaded by S. aureus. Recruitment of osteoclasts and other immunocytes plays a crucial role in the resorption and destruction of bone.

摘要

骨科感染难以治愈。金黄色葡萄球菌是导致骨科感染的主要病原体。金黄色葡萄球菌不仅能够定植于骨基质,还能侵入成骨细胞,这可能在骨髓炎的持续存在和复发中起重要作用。内化作用需要细胞骨架成分的参与,包括肌动蛋白微丝、微管和网格蛋白包被小窝。微丝在入侵过程中最为重要。金黄色葡萄球菌能够在成骨细胞中长期存活。对能够穿透宿主细胞的抗生素敏感性降低增加了根除金黄色葡萄球菌的难度。被金黄色葡萄球菌入侵的成骨细胞在炎症免疫反应的启动和维持中起重要作用。这些成骨细胞通过细胞因子的表达将白细胞和吞噬细胞募集到炎症部位。在被金黄色葡萄球菌入侵的成骨细胞中观察到细胞凋亡。破骨细胞和其他免疫细胞的募集在骨的吸收和破坏中起关键作用。