创伤环境巨噬细胞表型的时空相关性及其对生物材料 支架引导组织再生与修复的意义

doi:10.3969/j.issn.0258-8021. 2015. 04.012

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摘要炎症反应是机体对损伤和异物的正常应答，炎症的强度和持续时间影响生物材料在体内的相容性和稳定性。巨噬细胞是调控机体免疫和炎症反应的重要细胞，因此它对生物材料的响应性在认知材料-机体反应中有决定性作用。系统阐述巨噬细胞表型与机体创伤环境及对后期的修复和（或）再生、巨噬细胞表型与相关生物材料之间的相互作用，并对其未来发展方向进行评述。

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	郝绥绥许海燕^#*

关键词 ：巨噬细胞表型, 创伤环境, 生物材料, 修复, 再生

Abstract：The body inflammatory reaction is a normal response to injury and the presence of foreign substances.The duration and intensity of inflammation has a direct impact on biocompatibility and stability of biomaterials in vivo.Macrophage is one of the major cell types in controlling body inflammatory and immune processes,hence,its response to biomaterials is critical for identifying the biomaterialbody reaction.In this review, the correlation between macrophage phenotype and injury as well as the tissue repair or regeneration，the interaction of macrophages with biomaterials, and the future development are introduced in detail.

Key words： macrophages phenotype injury biomaterials;repair regeneration

基金资助:国家自然科学基金（81471793）

引用本文:

郝绥绥许海燕^#*. 创伤环境巨噬细胞表型的时空相关性及其对生物材料支架引导组织再生与修复的意义[J]. 中国生物医学工程学报, 2015, 34(4): 475-480.
Hao Suisui Xu Haiyan^{# *}. The Significance of Macrophage Phenotype in Injury as well as the Biomaterials Inducing Tissue Repair and Regeneration. journal1, 2015, 34(4): 475-480.

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http://cjbme.csbme.org/CN/10.3969/j.issn.0258-8021. 2015. 04.012 或 http://cjbme.csbme.org/CN/Y2015/V34/I4/475

［1］Bosco MC, Puppo M, Blengio F, et al.Monocytes and dendritic cells in a hypoxic environment: Spotlights on chemotaxis and migration［J］. Immunobiology，2008,213(9-10):733-749.
［2］Gordon S．Alternative activation of macrophages［J］.Nat Rev Immunol,2003,3(1):23-35．
［3］Mantovani A, Sica A, Sozzani S. The chemokine system in diverse forms of macrophage activation and polarization［J］.Trends Immunol,2004,25(12)：677-686．
［4］李丹，任亚娜，范华骅．巨噬细胞的分类及其调节性功能的差异［J］．生命科学，2011，22(3)：249-254．
［5］Summan M, Warren GL, Mercer RR, et al. Macrophages and skeletal muscle regeneration: a clodronatecontaining liposome depletion study［J］. Am J Physiol Regul Integr Comp Physiol, 2006, 290(6):R1488- R1495.
［6］Chazaud B, Brigitte M, YacoubYoussef H, et al.Dual and beneficial roles of macrophages during skeletal muscle regeneration ［J］. Exerc Sport Sci Rev, 2009,37(1):18-22.
［7］］Brigitte M, Schilte C, Plonquet A, et al. Muscle resident macrophages control the immune cell reaction in a mouse model of notexininduced myoinjury［J］.Arthritis Rheum,2010, 62(1): 268-279.
［8］Saclier M, YacoubYoussef H, Mackey AL, et al. Differentially activated macrophages orchestrate myogenic precursor cell fate during human skeletal muscle regeneration［J］. Stem Cells, 2013,31(2):384-396.
［9］Bencze M, Negroni E, Vallese D, et al.Proinflammatory macrophages enhance the regenerative capacity of human myoblasts by modifying their kinetics of proliferation and differentiation［J］. Mol Ther, 2012,20(11):2168-2179.
［10］Zamilpa R， Kanakia R， Cigarroa J，et al. CC chemokine receptor 5 deletion impairs macrophage activation and induces adverse remodeling following myocardial infarction［J］. Am J Physiol Heart Circ Physiol, 2011,300(4):H1418- H1426.
［11］Thorp EB. Mechanisms of failed apoptotic cell clearance by phagocyte subsets in cardiovascular disease［J］. Apoptosis, 2010,15(9):1124-1136.
［12］Zuidema MY, Zhang C. Ischemia/reperfusion injury: The role of immune cells［J］.World J Cardiol, 2010,2(10):325-332.
［13］Arslan F, Smeets MB, O〖DK〗’Neill LA, et al.Myocardial ischemia/reperfusion injury is mediated by leukocytic tolllike receptor2 and reduced by systemic administration of a novel antitolllike receptor2 antibody［J］.Circulation, 2010,121(1):80-90.
［14］Hori M, Nishida K. Oxidative stress and left ventricular remodelling after myocardial infarction［J］. Cardiovasc Res, 2009,81(3):457-464.
［15］Schwartz M, LazarovSpiegler O, Rapalino O, et al.Potential repair of rat spinal cord injuries using stimulated homologous macrophages ［J］. Neurosurgery,199944(5):1041-1045.
［16］George R, Griffin JW. Delayed macrophage responses and myelin clearance during Wallerian degeneration in the central nervous system: the dorsal radiculotomy model［J］. Exp Neurol, 1994,129(2):225-236.
［17］Hirschberg DL, Schwartz M. Macrophage recruitment to acutely injured central nervous system is inhibited by a resident factor: a basis for an immunebrain barrier［J］. J Neuroimmunol,1995,61(1):89-96.
［18］Lazarov-Spiegler O, Solomon AS, ZeevBrann AB, et al.Transplantation of activated macrophages overcomes central nervous system regrowth failure［J］.FASEB J,1996, 10(11): 1296-1302.
［19］Lazarov-Spiegler O, Solomon AS, Schwartz M. Link between optic nerve regrowth failure and macrophage stimulation in mammals ［J］. Vision Res,1999,39(1):169-175.
［20］Rapalino O, LazarovSpiegler O, Agranov E, et al.Implantation of stimulated homologous macrophages results in partial recovery of paraplegic rats［J］.Nat Med,19984(7): 814-821.
［21］Prewitt CM, Niesman IR, Kane CJ, et al. Activated macrophage/microglial cells can promote the regeneration of sensory axons into the injured spinal cord［J］.Exp Neurol, 1997, 148 (2) :433-443.
［22］Chamak B,Morandi V, Mallat M. Brain macrophages stimulate neurite growth and regeneration by secreting thrombospondin［J］.J Neurosci Res, 1994,38(2):221-233.
［23］Al-Mulla F, Leibovich SJ, Francis IM, et al. Impaired TGF\|β signaling and a defect in resolution of inflammation contribute to delayed wound healing in a female rat model of type 2 diabetes［J］.Mol Biosyst, 2011,7(11):3006-3020.
［24］Chang MK, Raggatt LJ, Alexander KA, et al. Osteal tissue macrophages are intercalated throughout human and mouse bone lining tissues and regulate osteoblast function in vitro and in vivo［J］. J Immunol, 2008,181(2):1232-1244.
［25］Raggatt LJ, Wullschleger ME, Alexander KA, et al. Fracture healing via periosteal callus formation requires macrophages for both initiation and progression of early endochondral ossification［J］. Am J Pathol, 2014,184(12):3192-3204.
［26］Montesinos MC, Shaw JP, Yee H, et al. Adenosine A(2A) receptor activation promotes wound neovascularization by stimulating angiogenesis and vasculogenesis［J］.Am J Pathol,2004, 164(6):1887-1892.
［27］Pinhal-Enfield G, Ramanathan M, Hasko G, et al. An angiogenic switch in macrophages involving synergy between Tolllike receptors 2, 4, 7, and 9 and adenosine A(2A) receptors［J］. Am J Pathol, 2003, 163(2):711-721.
［28］Chen Jianxiong, Chen Ying, DeBusk L, et al. Dual functional roles of Tie-2/angiopoietin in TNFalphamediated angiogenesis ［J］.Am J Physiol Heart Circ Physiol, 2004287(1):H187- H195.
［29］Spiller KL, Anfang RR, Spiller KJ, et al.The role of macrophage phenotype in vascularization of tissue engineering scaffolds ［J］.Biomaterials,2014,35(15):4477-4488.
［30］Yao Kangde, Yin Yuji. Biomaterials Related Tissue Engineering ［M］. Beijing: Chemical Industry Press,2003: 255-256.
［31］Mikos AG, McIntire LV, Anderson JM, et al. Host response to tissue engineered devices［J］.Adv Drug Deliv Rev, 1998,33(1-2):111-139.
［32］Anderson JM．Biological responses to materials［J］.Annual Review of Materials Research,2001, 31:81-110.
［33］Brodbeck WG, Nakayama Y, Matsuda T, et al.Biomaterial surface chemistry dictates adherent monocyte/macrophage cytokine expression in vitro［J］.Cytokine,200218(6):311-319.
［34］Brodbeck WG, Voskerician G, Ziats NP, et al. In vivo leukocyte cytokine mRNA responses to biomaterials are dependent on surface chemistry［J］.J Biomed Mater Res A, 2003,64(2):320-329.
［35］Kao WJ, Lee D, Schense JC, Hubbell JA. Fibronectin modulates macrophage adhesion and FBGC formation: the role of RGD, PHSRN, and PRRARV domains［J］. J Biomed Mater Res, 2001,55(1):79-88.
［36］Kao WJ，Lee DM. In vivo modulation of host response and macrophage behavior by polymer networks grafted with fibronectin derived biomimetic oligopeptides：the role of RGD and PHSRN domain［J］.Biomaterials,2001,22: 2901-2909.
［37］Rose SF, Lewis AL, Hanlon GW, et al. Biological responses to cationically charged phosphorylcholinebased materials in vitro ［J］. Biomaterials,2004,25(21):5125-5135.
［38］Spiller KL, Anfang RR, Spiller KJ, et al.The role of macrophage phenotype in vascularization of tissue engineering scaffolds ［J］. Biomaterials,2014, 35〖(15):4477-4488.
［39］Hiroshi U，Takashi M，Toru F. Topical formulations and wound healing applications of chitosan ［J］.Advanced Drug Delivery Reviews, 2001, 52: 105-115.
［40］Feng Jie，Zhao Luhang，Yu Qiqi. Receptormediated stimulatory effect of oligo chitosan in macrophages ［J］.Biochem Biophys Res Commun, 2004,317(2):414-420. 
［41］Anderson JM,Rodriguez A,Chang DT. Foreign body reaction to biomaterials［J］.Semin Immunol, 2008,20(2):86-100.
［42］Martinez FO,Helming L,Gordon S. Alternative activation of macrophages: an immunologic functional perspective［J］.Annu Rev Immunol, 2009,27:451-483.
［43］Varin A,Gordon S. Alternative activation of macrophages: immune function and cellular biology［J］.Immunobiology, 2009,214(7):630-641.
［44］Madden LR, Mortisen DJ, Sussman EM, et al. Proangiogenic scaffolds as functional templates for cardiac tissue engineering［J］.Proc Natl Acad Sci USA,2010,107(34):15211-15216.
［45］Garg K, Pullen NA, Oskeritzian CA, et al. Macrophage functional polarization (M1/M2) in response to varying fiber and pore dimensions of electrospun scaffolds［J］.Biomaterials,2013, 34(18): 4439-4451.
［46］Yang Zaifu, Yang Jinggen, Gao Guanghuang. The review of the action of immune modulation of lowintensity laser ［J］.Chin J Phys Ther, 2001, 24 (4): 244-247.
［47］徐朝阳,谭石慈,邢达, 等.HeNe激光照射巨噬细胞对胞内钙浓度及其免疫活性的影响［J］.中国激光,2004,31(2):253-256.
［48］ Kao CH, Chen JJ, Hsu YM, et al.Highfrequency electrical stimulation can be a complementary therapy to promote nerve regeneration in diabetic rats［J］.PLoS ONE,2013,8(11): e79078.
［49］Ross CL, Harrison BS. Effect of pulsed electromagnetic field on inflammatory pathway markers in RAW 2647 murine macrophages ［J］.J Inflamm Res,2013,6:45-51.
［50］Selvam R, Ganesan K, Narayana Raju KV, et al. Low frequency and low intensity pulsed electromagnetic field exerts its antiinflammatory effect through restoration of plasma membrane calcium ATPase activity［J］.Life Sci, 2007,80 (26): 2403-2410.
［51］Shiratsuchi H, Basson MD. Extracellular pressure stimulates macrophage phagocytosis by inhibiting a pathway involving FAK and ERK［J］.Am J Physiol Cell Physiol, 2004, 286 (6): C1358-C1366.
［52］Sakamoto H, Aikawa M, Hill CC, et al. Biomechanical strain induces class A scavenger receptor expression in human monocyte/macrophages and THP\|1 cells. A potential mechanism of increased atherosclerosis in hypertension［J］.Circulation,2001, 104: 109-114.