RESEARCH PROGRESS OF IMMUNO-INFLAMMATORY RESPONSE AND PATHOLOGICAL SCAR_Chinese Journal of Reparative and Reconstructive Surgery

Authors：

CHENYan , XIELihong ,  ZHANGJie , FUJianhua

Department of Aesthetic Plastic Surgery, the First Affiliated Hospital of Nanchang University, Nanchang Jiangxi, 330006, P. R. China;

Corresponding author：

ZHANGJie, Email: zhjprs@163.com

Keywords：

Pathological scar; Formation mechanism; Inflammation response; Immune response

DOI：

10.7507/1002-1892.20150137

Video：

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Objective To review the research progress of the roles of inflammation and immune response in the formation of pathological scar. Methods The recent literature concerning the formation mechanism of pathological scar was extensively consulted, inflammation and immune response involved in the formation of pathological scar was reviewed. Results The formation of pathological scar is associated with inflammation and immune response, some inflammatory factors will promote the activation of immune cells, then induce immune cells releasing cytokines and aggravate inflammatory response. However, inflammation response also affects the level of immune response. So they work together to promote the formation of pathological scar by the immuno-inflammatory cells and media. Conclusion The formation of pathological scar is not only related to inflammation response, but also involves in immune response. Moreover, immune response is the new progress in the study of pathological scar mechanism in recent years. Further research of immuno-inflammatory response will provide new ideas and corresponding basis for the prevention of pathological scar.

Citation： CHENYan, XIELihong, ZHANGJie, FUJianhua. RESEARCH PROGRESS OF IMMUNO-INFLAMMATORY RESPONSE AND PATHOLOGICAL SCAR. Chinese Journal of Reparative and Reconstructive Surgery, 2015, 29(5): 640-644. doi: 10.7507/1002-1892.20150137 Copy

1.	Gurtner GC, Werner S, Barrandon Y, et al. Wound repair and regeneration. Nature, 2008, 453(7193):314-321.
2.	Gauglitz GG, Korting HC, Pavicic T, et al. Hypertrophic scarring and keloids:pathomechanisms and current and emerging treatment strategies. Mol Med, 2011, 17(1-2):113-125.
3.	Eming SA, Martin P, Tomic-Canic M. Wound repair and regeneration:mechanisms, signaling, and translation. Sci Transl Med, 2014, 6(265):265sr6.
4.	Sun BK, Siprashvili Z, Khavari PA. Advances in skin grafting and treatment of cutaneous wounds. Science, 2014, 346(6212):941-945.
5.	Martin P, Leibovich SJ. Inflammatory cells during wound repair:the good, the bad and the ugly. Trends Cell Biol, 2005, 15(11):599-607.
6.	Martin P, D'Souza D, Martin J, et al. Wound healing in the PU.1 null mouse-tissue repair is not dependent on inflammatory cells. Curr Biol, 2003, 13(13):1122-1128.
7.	Mahdavian Delavary B, van der Veer WM, van Egmond M, et al. Macrophages in skin injury and repair. Immunobiology, 2011, 216(7):753-762.
8.	Huang C, Murphy GF, Akaishi S, et al. Keloids and hypertrophic scars:update and future directions. Plast Reconstr Surg Glob Open, 2013, 1(4):e25.
9.	Zgheib C, Xu J, Liechty KW. Targeting inflammatory cytokines and extracellular matrix composition to promote wound regeneration. Adv Wound Care (New Rochelle), 2014, 3(4):344-355.
10.	Caskey RC, Allukian M, Lind RC, et al. Lentiviral-mediated over-expression of hyaluronan synthase-1 (HAS-1) decreases the cellular inflammatory response and results in regenerative wound repair. Cell Tissue Res, 2013, 351(1):117-125.
11.	Lim AF, Weintraub J, Kaplan EN, et al. The embrace device significantly decreases scarring following scar revision surgery in a randomized controlled trial. Plast Reconstr Surg, 2014, 133(2):398-405.
12.	Wong VW, Paterno J, Sorkin M, et al. Mechanical force prolongs acute inflammation via T-cell-dependent pathways during scar formation. FASEB J, 2011, 25(12):4498-4510.
13.	Ud-Din S, Volk SW, Bayat A. Regenerative healing, scar-free healing and scar formation across the species:current concepts and future perspectives. Exp Dermatol, 2014, 23(9):615-619.
14.	van den Broek LJ, Limandjaja GC, Niessen FB, et al. Human hypertrophic and keloid scar models:principles, limitations and future challenges from a tissue engineering perspective. Exp Dermatol, 2014, 23(6):382-386.
15.	Song C. Hypertrophic scars and keloids in surgery:current concepts. Ann Plast Surg, 2014, 73 Suppl 1:S108-S118.
16.	Glim JE, Beelen RH, Niessen FB, et al. The number of immune cells is lower in healthy oral mucosa compared to skin and does not increase after scarring. Arch Oral Biol, 2015, 60(2):272-281.
17.	Brown JJ, Bayat A. Genetic susceptibility to raised dermal scarring. Br J Dermatol, 2009, 161(1):8-18.
18.	Pistorio AL, Ehrlich HP. Modulatory effects of connexin-43 expression on gap junction intercellular communications with mast cells and fibroblasts. J Cell Biochem, 2011, 112(5):1441-1449.
19.	Foley TT, Saggers GC, Moyer KE, et al. Rat mast cells enhance fibroblast proliferation and fibroblast-populated collagen lattice contraction through gap junctional intercellular communications. Plast Reconstr Surg, 2011, 127(4):1478-1486.
20.	Kieran I, Knock A, Bush J, et al. Interleukin-10 reduces scar formation in both animal and human cutaneous wounds:results of two preclinical and phase Ⅱ randomized control studies. Wound Repair Regen, 2013, 21(3):428-436.
21.	King A, Balaji S, Le LD, et al. Regenerative wound healing:the role of interleukin-10. Adv Wound Care (New Rochelle), 2014, 3(4):315-323.
22.	Tan KT, McGrrouther DA, Day AJ, et al. Characterization of hyaluronan and TSG-6 in skin scarring:differential distribution in keloid scar, normal scar and unscarred skin. J Eur Acad Dermatol Venereol, 2011, 25(3):317-327.
23.	Wang H, Chen Z, Li XJ, et al. Anti-inflammatory cytokine TSG-6 inhibits hypertrophic scar formation in a rabbit ear model. Eur J Pharmacol, 2015, 751:42-49.
24.	Márquez García A, Ojeda Vila T, Ferrándiz L, et al. Hypertrophic and keloid scars after the application of 5% imiquimod cream:a report of 2 cases. Actas Dermosifiliogr, 2014, 105(8):795-797.
25.	Chen L, Schrementi ME, Ranzer MJ, et al. Blockade of mast cell activation reduces cutaneous scar formation. PLoS One, 2014, 9(1):e85226.
26.	Sandulache VC, Parekh A, Li-Korotky H, et al. Prostaglandin E2 inhibition of keloid fibroblast migration, contraction, and transforming growth factor (TGF)-beta1-induced collagen synthesis. Wound Repair Regen, 2007, 15(1):122-133.
27.	Li F, Huang Q, Chen J, et al. Apoptotic cells activate the "phoenix rising" pathway to promote wound healing and tissue regeneration. Sci Signal, 2010, 3(110):ra13.
28.	Lee RH, Pulin AA, Seo MJ, et al. Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6. Cell Stem Cell, 2009, 5(1):54-63.
29.	Roddy GW, Oh JY, Lee RH, et al. Action at a distance:systemically administered adult stem/progenitor cells (MSCs) reduce inflammatory damage to the cornea without engraftment and primarily by secretion of TNF-α stimulated gene/protein 6. Stem Cells, 2011, 29(10):1572-1579.
30.	Mora-Lee S, Sirerol-Piquer MS, Gutierrez-Perez M, et al. Therapeutic effects of hMAPC and hMSC transplantation after stroke in mice. PLoS One, 2012, 7(8):e43683.
31.	Liang Q, Liu S, Han P, et al. Micronized acellular dermal matrix as an efficient expansion substrate and delivery vehicle of adipose-derived stem cells for vocal fold regeneration. Laryngoscope, 2012, 122(8):1815-1825.
32.	Jackson WM, Nesti LJ, Tuan RS. Mesenchymal stem cell therapy for attenuation of scar formation during wound healing. Stem Cell Res Ther, 2012, 3(3):20.
33.	Le Blanc K, Mougiakakos D. Multipotent mesenchymal stromal cells and the innate immune system. Nat Rev Immunol, 2012, 12(5):383-396.
34.	Liu S, Jiang L, Li H, et al. Mesenchymal stem cells prevent hypertrophic scar formation via inflammatory regulation when undergoing apoptosis. J Invest Dermatol, 2014, 134(10):2648-2657.
35.	Qi Y, Jiang D, Sindrilaru A, et al. TSG-6 released from intradermally injected mesenchymal stem cells accelerates wound healing and reduces tissue fibrosis in murine full-thickness skin wounds. J Invest Dermatol, 2014, 134(2):526-537.

1. Gurtner GC, Werner S, Barrandon Y, et al. Wound repair and regeneration. Nature, 2008, 453(7193):314-321.
2. Gauglitz GG, Korting HC, Pavicic T, et al. Hypertrophic scarring and keloids:pathomechanisms and current and emerging treatment strategies. Mol Med, 2011, 17(1-2):113-125.
3. Eming SA, Martin P, Tomic-Canic M. Wound repair and regeneration:mechanisms, signaling, and translation. Sci Transl Med, 2014, 6(265):265sr6.
4. Sun BK, Siprashvili Z, Khavari PA. Advances in skin grafting and treatment of cutaneous wounds. Science, 2014, 346(6212):941-945.
5. Martin P, Leibovich SJ. Inflammatory cells during wound repair:the good, the bad and the ugly. Trends Cell Biol, 2005, 15(11):599-607.
6. Martin P, D'Souza D, Martin J, et al. Wound healing in the PU.1 null mouse-tissue repair is not dependent on inflammatory cells. Curr Biol, 2003, 13(13):1122-1128.
7. Mahdavian Delavary B, van der Veer WM, van Egmond M, et al. Macrophages in skin injury and repair. Immunobiology, 2011, 216(7):753-762.
8. Huang C, Murphy GF, Akaishi S, et al. Keloids and hypertrophic scars:update and future directions. Plast Reconstr Surg Glob Open, 2013, 1(4):e25.
9. Zgheib C, Xu J, Liechty KW. Targeting inflammatory cytokines and extracellular matrix composition to promote wound regeneration. Adv Wound Care (New Rochelle), 2014, 3(4):344-355.
10. Caskey RC, Allukian M, Lind RC, et al. Lentiviral-mediated over-expression of hyaluronan synthase-1 (HAS-1) decreases the cellular inflammatory response and results in regenerative wound repair. Cell Tissue Res, 2013, 351(1):117-125.
11. Lim AF, Weintraub J, Kaplan EN, et al. The embrace device significantly decreases scarring following scar revision surgery in a randomized controlled trial. Plast Reconstr Surg, 2014, 133(2):398-405.
12. Wong VW, Paterno J, Sorkin M, et al. Mechanical force prolongs acute inflammation via T-cell-dependent pathways during scar formation. FASEB J, 2011, 25(12):4498-4510.
13. Ud-Din S, Volk SW, Bayat A. Regenerative healing, scar-free healing and scar formation across the species:current concepts and future perspectives. Exp Dermatol, 2014, 23(9):615-619.
14. van den Broek LJ, Limandjaja GC, Niessen FB, et al. Human hypertrophic and keloid scar models:principles, limitations and future challenges from a tissue engineering perspective. Exp Dermatol, 2014, 23(6):382-386.
15. Song C. Hypertrophic scars and keloids in surgery:current concepts. Ann Plast Surg, 2014, 73 Suppl 1:S108-S118.
16. Glim JE, Beelen RH, Niessen FB, et al. The number of immune cells is lower in healthy oral mucosa compared to skin and does not increase after scarring. Arch Oral Biol, 2015, 60(2):272-281.
17. Brown JJ, Bayat A. Genetic susceptibility to raised dermal scarring. Br J Dermatol, 2009, 161(1):8-18.
18. Pistorio AL, Ehrlich HP. Modulatory effects of connexin-43 expression on gap junction intercellular communications with mast cells and fibroblasts. J Cell Biochem, 2011, 112(5):1441-1449.
19. Foley TT, Saggers GC, Moyer KE, et al. Rat mast cells enhance fibroblast proliferation and fibroblast-populated collagen lattice contraction through gap junctional intercellular communications. Plast Reconstr Surg, 2011, 127(4):1478-1486.
20. Kieran I, Knock A, Bush J, et al. Interleukin-10 reduces scar formation in both animal and human cutaneous wounds:results of two preclinical and phase Ⅱ randomized control studies. Wound Repair Regen, 2013, 21(3):428-436.
21. King A, Balaji S, Le LD, et al. Regenerative wound healing:the role of interleukin-10. Adv Wound Care (New Rochelle), 2014, 3(4):315-323.
22. Tan KT, McGrrouther DA, Day AJ, et al. Characterization of hyaluronan and TSG-6 in skin scarring:differential distribution in keloid scar, normal scar and unscarred skin. J Eur Acad Dermatol Venereol, 2011, 25(3):317-327.
23. Wang H, Chen Z, Li XJ, et al. Anti-inflammatory cytokine TSG-6 inhibits hypertrophic scar formation in a rabbit ear model. Eur J Pharmacol, 2015, 751:42-49.
24. Márquez García A, Ojeda Vila T, Ferrándiz L, et al. Hypertrophic and keloid scars after the application of 5% imiquimod cream:a report of 2 cases. Actas Dermosifiliogr, 2014, 105(8):795-797.
25. Chen L, Schrementi ME, Ranzer MJ, et al. Blockade of mast cell activation reduces cutaneous scar formation. PLoS One, 2014, 9(1):e85226.
26. Sandulache VC, Parekh A, Li-Korotky H, et al. Prostaglandin E2 inhibition of keloid fibroblast migration, contraction, and transforming growth factor (TGF)-beta1-induced collagen synthesis. Wound Repair Regen, 2007, 15(1):122-133.
27. Li F, Huang Q, Chen J, et al. Apoptotic cells activate the "phoenix rising" pathway to promote wound healing and tissue regeneration. Sci Signal, 2010, 3(110):ra13.
28. Lee RH, Pulin AA, Seo MJ, et al. Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6. Cell Stem Cell, 2009, 5(1):54-63.
29. Roddy GW, Oh JY, Lee RH, et al. Action at a distance:systemically administered adult stem/progenitor cells (MSCs) reduce inflammatory damage to the cornea without engraftment and primarily by secretion of TNF-α stimulated gene/protein 6. Stem Cells, 2011, 29(10):1572-1579.
30. Mora-Lee S, Sirerol-Piquer MS, Gutierrez-Perez M, et al. Therapeutic effects of hMAPC and hMSC transplantation after stroke in mice. PLoS One, 2012, 7(8):e43683.
31. Liang Q, Liu S, Han P, et al. Micronized acellular dermal matrix as an efficient expansion substrate and delivery vehicle of adipose-derived stem cells for vocal fold regeneration. Laryngoscope, 2012, 122(8):1815-1825.
32. Jackson WM, Nesti LJ, Tuan RS. Mesenchymal stem cell therapy for attenuation of scar formation during wound healing. Stem Cell Res Ther, 2012, 3(3):20.
33. Le Blanc K, Mougiakakos D. Multipotent mesenchymal stromal cells and the innate immune system. Nat Rev Immunol, 2012, 12(5):383-396.
34. Liu S, Jiang L, Li H, et al. Mesenchymal stem cells prevent hypertrophic scar formation via inflammatory regulation when undergoing apoptosis. J Invest Dermatol, 2014, 134(10):2648-2657.
35. Qi Y, Jiang D, Sindrilaru A, et al. TSG-6 released from intradermally injected mesenchymal stem cells accelerates wound healing and reduces tissue fibrosis in murine full-thickness skin wounds. J Invest Dermatol, 2014, 134(2):526-537.

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