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Harnessing strategies for enhancing diabetic wound healing from the perspective of spatial inflammation patterns

Cai, Yixin, Chen, Kangli, Liu, Changsheng, Qu, Xue·2023·Bioactive Materials
DOI 10.1016/j.bioactmat.2023.04.019PMC PMC10245071
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Fig. 1 (A) The causative reason for the non-healing diabetic wound is immune dysfunction in the inflammatory phase, which makes the diabetic wound healing process fail to enter the proliferation phase. (B) To enhance the diabetic wound healing process, inhibiting inflammatory response to avoid subsequent immune cell infiltration and fostering a supportive physiological condition for wound repairing is feasible for the early-wound pattern. When an excessive and persistent inflammation pattern is established in long-term non-healing wound, one strategy is about changing chronic wounds to acute, which aims to normalize abnormal M1 macrophage and make its polarization spontaneously, another strategy is about employing switches for M1/M2 transition. All of these strategies lead to the proliferation phase.
Fig. 1 (A) The causative reason for the non-healing diabetic wound is immune dysfunction in the inflammatory phase, which makes the diabetic wound healing process fail to enter the proliferation phase. (B) To enhance the diabetic wound healing process, inhibiting inflammatory response to avoid subsequent immune cell infiltration and fostering a supportive physiological condition for wound repairing is feasible for the early-wound pattern. When an excessive and persistent inflammation pattern is established in long-term non-healing wound, one strategy is about changing chronic wounds to acute, which aims to normalize abnormal M1 macrophage and make its polarization spontaneously, another strategy is about employing switches for M1/M2 transition. All of these strategies lead to the proliferation phase.CC BY-NC-ND · PubMed Central
Fig. 2 Scheme of reasons for impaired M1/M2 transition in diabetic wound healing, it includes (A) a positive feedback loop of M1 accumulation, (B) impaired M1 phagocytotic activity, and (C) more senescent M1. (A) Diabetic wounds are usually stuck in an excessive inflammatory state with IL-1β, IL-6, TNF, IL-12, IL-18, etc. Among these inflammatory molecules, IL-1β, IL-6, and TNF are signals that recruit monocytes to the wounded region. Subsequently, the recruited monocytes polarize to the M1 phenotype with the guide of IL-12 and IL-18 in the wound bed and secrete monocyte recruiting signals. (B) M1 in normal wound healing is robust with a powerful capacity of clearing apoptotic cell debris and the process of phagocytosis aids the occurrence of M1/M2 transition. M1 in diabetic wound healing is abnormal with decreased receptors for phagocytosis, which leads to limited phagocytotic capacity and reduced M2 polarization. (C) Compared to the spontaneous occurrence of M1/M2 transition in normal wound healing, M1 macrophges are abnormal with more senescent phenotypes, accompanied by shrinking plasticity that hinders M1/M2 transition. Senescent-Associated Secrectory Profile (SASP) is a significant feature of senescent cells.
Fig. 2 Scheme of reasons for impaired M1/M2 transition in diabetic wound healing, it includes (A) a positive feedback loop of M1 accumulation, (B) impaired M1 phagocytotic activity, and (C) more senescent M1. (A) Diabetic wounds are usually stuck in an excessive inflammatory state with IL-1β, IL-6, TNF, IL-12, IL-18, etc. Among these inflammatory molecules, IL-1β, IL-6, and TNF are signals that recruit monocytes to the wounded region. Subsequently, the recruited monocytes polarize to the M1 phenotype with the guide of IL-12 and IL-18 in the wound bed and secrete monocyte recruiting signals. (B) M1 in normal wound healing is robust with a powerful capacity of clearing apoptotic cell debris and the process of phagocytosis aids the occurrence of M1/M2 transition. M1 in diabetic wound healing is abnormal with decreased receptors for phagocytosis, which leads to limited phagocytotic capacity and reduced M2 polarization. (C) Compared to the spontaneous occurrence of M1/M2 transition in normal wound healing, M1 macrophges are abnormal with more senescent phenotypes, accompanied by shrinking plasticity that hinders M1/M2 transition. Senescent-Associated Secrectory Profile (SASP) is a significant feature of senescent cells.CC BY-NC-ND · PubMed Central
Fig. 3 (A) Inhibiting proinflammatory response at the early diabetic wound to avoid subsequent persistent and excessive immune process fosters a favorable condition for wound healing, thus wound healing process enters the proliferation phase. (B) Full-thickness excisional wound with a diameter of 2 mm is made in wide-type mice and PU.1 null mice. Macrophages and neutrophils are depleted genetically in PU.1 null mice. Wild-type mice and PU.1 null mice show similar time course of wound repair at 7 days post-wounding. Especially, tissue repair in PU.1 mice is more effective and appears scar-free. (C–F) and (G–H) are two cases about designing biomaterials for inhibiting proinflammatory response. (C) Resident immune cells establish a chemokine gradient that attracts neutrophils and monocytes from circulating system. A hydrogel that captures chemoattractant (MCP-1 and IL-β) is designed for cutting off the signal for neutrophil and monocyte infiltration. (D–F) Full-thickness injury in db/db mice treated with promogran (FDA-approved hydrogel-based wound dressing) or PEG/N-dSH (the chemoattractant-capturing hydrogel). (D) Concentration of MCP-1 in PEG/N-dSH hydrogel increases from 5 day to 10 day post-wounding (dpw). (E) Concentrations of MCP-1 and IL-1β in wound bed at 10 dpw suggest alleviated inflammatory response during wound healing. e, epidermis; f, fat tissue; g, granulation tissue. Arrowhead points to epithelial tip. (F) Immunofluorescence staining of newly formed tissue indicates faster reepithelialization with the treatment of PEG/N-dSH hydrogel. (G) The dual-action TCP-25 peptide contained in the hydrogel, not only binds to neutrophils, making neutrophils inaccessible to bacteria, but also has the ability to kill the bacteria itself. (H) In the presence of TCP-25 containing hydrogel, LPS-induced inflammatory response is reduced in chronic wound fluid from five patients. Scale bar: 100 μm for (B), 200 μm for (F). Reprinted with permission from Ref.65. Copyright 2003 Elsevier. Reprinted with permission from Ref.67. Copyright 2017 The American Association for the Advancement of Science. Reprinted with permission from Ref.68. Copyright 2020 The American Association for the Advancement of Science.
Fig. 3 (A) Inhibiting proinflammatory response at the early diabetic wound to avoid subsequent persistent and excessive immune process fosters a favorable condition for wound healing, thus wound healing process enters the proliferation phase. (B) Full-thickness excisional wound with a diameter of 2 mm is made in wide-type mice and PU.1 null mice. Macrophages and neutrophils are depleted genetically in PU.1 null mice. Wild-type mice and PU.1 null mice show similar time course of wound repair at 7 days post-wounding. Especially, tissue repair in PU.1 mice is more effective and appears scar-free. (C–F) and (G–H) are two cases about designing biomaterials for inhibiting proinflammatory response. (C) Resident immune cells establish a chemokine gradient that attracts neutrophils and monocytes from circulating system. A hydrogel that captures chemoattractant (MCP-1 and IL-β) is designed for cutting off the signal for neutrophil and monocyte infiltration. (D–F) Full-thickness injury in db/db mice treated with promogran (FDA-approved hydrogel-based wound dressing) or PEG/N-dSH (the chemoattractant-capturing hydrogel). (D) Concentration of MCP-1 in PEG/N-dSH hydrogel increases from 5 day to 10 day post-wounding (dpw). (E) Concentrations of MCP-1 and IL-1β in wound bed at 10 dpw suggest alleviated inflammatory response during wound healing. e, epidermis; f, fat tissue; g, granulation tissue. Arrowhead points to epithelial tip. (F) Immunofluorescence staining of newly formed tissue indicates faster reepithelialization with the treatment of PEG/N-dSH hydrogel. (G) The dual-action TCP-25 peptide contained in the hydrogel, not only binds to neutrophils, making neutrophils inaccessible to bacteria, but also has the ability to kill the bacteria itself. (H) In the presence of TCP-25 containing hydrogel, LPS-induced inflammatory response is reduced in chronic wound fluid from five patients. Scale bar: 100 μm for (B), 200 μm for (F). Reprinted with permission from Ref.65. Copyright 2003 Elsevier. Reprinted with permission from Ref.67. Copyright 2017 The American Association for the Advancement of Science. Reprinted with permission from Ref.68. Copyright 2020 The American Association for the Advancement of Science.CC BY-NC-ND · PubMed Central
Fig. 4 (A) Scheme of changing chronic wound to acute in the long-term non-healing wound, which aims to normalize M1 macrophages and make the spontaneous M1/M2 transition. (B–D) Delivering proinflammatory molecules such as (B) SDF-1, (C)PLG, and (D) SP in western medicine strategy rescued the non-healing diabetic wound. (B) Samples at day 28 post-wounding. Scale bar: 50 μm. (C) Samples at day 14 post-wounding. Green arrow pointed to epithelialization, white arrow pointed to mild angiogenesis, red arrow pointed to hair follicle, yellow arrow pointed to connective tissue. Scale bar: 100 μm. (D) Samples at day 10 post-wounding. (E) A full-thickness injury measuring 1.8 cm*1.8 cm was created in diabetic mice and treated with a traditional Chinese medicine wound dressing, Wenyangyiqi formula. The H&E staining (100 magnifications) showed more immune cell infiltration at day 3 and day 7 treated with Wenyangyiqi formula. Few newly vessels, collagen fibers, and fibroblasts appeared at day 7 treated with Wenyagyiqi formula. In addition to alleviated inflammation, mature epithelial layer were observed at day 14 treated with Wenyangyiqi formula. Reprinted with permission from Ref.83. Copyright 2021 American Chemical Society. Reprinted with permission from Ref.88. Copyright 2022 MDPI. Reprinted with permission from Ref.45. Copyright 2015 Elsevier. Reprinted with permission from Ref.96. Copyright 2021 CNKI.
Fig. 4 (A) Scheme of changing chronic wound to acute in the long-term non-healing wound, which aims to normalize M1 macrophages and make the spontaneous M1/M2 transition. (B–D) Delivering proinflammatory molecules such as (B) SDF-1, (C)PLG, and (D) SP in western medicine strategy rescued the non-healing diabetic wound. (B) Samples at day 28 post-wounding. Scale bar: 50 μm. (C) Samples at day 14 post-wounding. Green arrow pointed to epithelialization, white arrow pointed to mild angiogenesis, red arrow pointed to hair follicle, yellow arrow pointed to connective tissue. Scale bar: 100 μm. (D) Samples at day 10 post-wounding. (E) A full-thickness injury measuring 1.8 cm*1.8 cm was created in diabetic mice and treated with a traditional Chinese medicine wound dressing, Wenyangyiqi formula. The H&E staining (100 magnifications) showed more immune cell infiltration at day 3 and day 7 treated with Wenyangyiqi formula. Few newly vessels, collagen fibers, and fibroblasts appeared at day 7 treated with Wenyagyiqi formula. In addition to alleviated inflammation, mature epithelial layer were observed at day 14 treated with Wenyangyiqi formula. Reprinted with permission from Ref.83. Copyright 2021 American Chemical Society. Reprinted with permission from Ref.88. Copyright 2022 MDPI. Reprinted with permission from Ref.45. Copyright 2015 Elsevier. Reprinted with permission from Ref.96. Copyright 2021 CNKI.CC BY-NC-ND · PubMed Central
Fig. 5 (A) Scheme of switches for M1/M2 transition to enhance diabetic wound healing. (B–D) Extracellular vesicles (EVs)-based switches. (B) Calreticulin exposed on the surface of EVs functions as “eat me” signal. The uptake of EVs guides the reprogramming of M1 macropahge to M2 phenotype. (C) The uptake of apoptotic vesicles (apoV, a member belonging to EVs family) by bone marrow-derived macrophage (BMDM). Scale bar: 20 μm (D) The treatment of apoV reprogrammed M1 to M2 phenotype in diabetic mice. Ctrl, control mice. DIO, diet-induced obesity mice. apoV, DIO mice treated with apoV. Scale bar: 50 μm. (E–H) Biomaterial-base switches for M1/M2 transition including (E) pores, (F) stiffness, and (G) surface topography. (E) Electrospun with varying concentrations of polydioxanone (60,100,140 mg/ml), higher concentration generated larger fiber with increased pore size. Macrophages prime to express more M1 marker iNOS in smaller pores and more M2 marker Arg in larger pores. (F) Macrophages prime pro-inflammatory phenotype on stiffer substrate and anti-inflammatory phenotype on softer substrate. Macrophages acquired the mechanical information of biomaterials by TLR4. M0 medium: with no induction factor. M1 medium: IFN + LPS induction. M2 medium: IL4+IL13 induction. TNF, MIP1α, IL-6, CCL20, and CXCL11 are pro-inflammatory expressions. IL10, CCL22, CCL17, and CCL13 are anti-inflammatory expressions. (G) Macrophages prime rounded M1 phenotype with the expression of iNOS on unpatterned surface and elongated M2 phenotype with the expression of Arg on microgrooved surface. Scale bar: 50 μm. Reprinted with permission from Ref.106. Copyright 2021 John Wiley and Sons. Reprinted with permission from Ref.111. Copyright 2013 Elsevier. Reprinted with permission from Ref.117. Copyright 2019 Elsevier. Reprinted with permission from Ref.123. Copyright 2013 NAS.
Fig. 5 (A) Scheme of switches for M1/M2 transition to enhance diabetic wound healing. (B–D) Extracellular vesicles (EVs)-based switches. (B) Calreticulin exposed on the surface of EVs functions as “eat me” signal. The uptake of EVs guides the reprogramming of M1 macropahge to M2 phenotype. (C) The uptake of apoptotic vesicles (apoV, a member belonging to EVs family) by bone marrow-derived macrophage (BMDM). Scale bar: 20 μm (D) The treatment of apoV reprogrammed M1 to M2 phenotype in diabetic mice. Ctrl, control mice. DIO, diet-induced obesity mice. apoV, DIO mice treated with apoV. Scale bar: 50 μm. (E–H) Biomaterial-base switches for M1/M2 transition including (E) pores, (F) stiffness, and (G) surface topography. (E) Electrospun with varying concentrations of polydioxanone (60,100,140 mg/ml), higher concentration generated larger fiber with increased pore size. Macrophages prime to express more M1 marker iNOS in smaller pores and more M2 marker Arg in larger pores. (F) Macrophages prime pro-inflammatory phenotype on stiffer substrate and anti-inflammatory phenotype on softer substrate. Macrophages acquired the mechanical information of biomaterials by TLR4. M0 medium: with no induction factor. M1 medium: IFN + LPS induction. M2 medium: IL4+IL13 induction. TNF, MIP1α, IL-6, CCL20, and CXCL11 are pro-inflammatory expressions. IL10, CCL22, CCL17, and CCL13 are anti-inflammatory expressions. (G) Macrophages prime rounded M1 phenotype with the expression of iNOS on unpatterned surface and elongated M2 phenotype with the expression of Arg on microgrooved surface. Scale bar: 50 μm. Reprinted with permission from Ref.106. Copyright 2021 John Wiley and Sons. Reprinted with permission from Ref.111. Copyright 2013 Elsevier. Reprinted with permission from Ref.117. Copyright 2019 Elsevier. Reprinted with permission from Ref.123. Copyright 2013 NAS.CC BY-NC-ND · PubMed Central

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Metadata

Authors
Cai, Y., Chen, K., Liu, C., & Qu, X.
ORCID
Qu, Xue
Venue
Bioactive Materials
Publisher
Elsevier BV
Published
2023-10
Volume
28
Pages
243-254
ISSN
2452-199X
DOI
10.1016/j.bioactmat.2023.04.019
PMC
PMC10245071
Cited by
112
References
13
Language
en
Licence
Funders
  • Higher Education Discipline Innovation Project (B14018)
  • Science and Technology Project of Nantong City
  • National Natural Science Foundation of China National Outstanding Youth Science Fund Project (11932012, 31922041, 32171341)
  • National Key Research and Development Program of China (2021YFB3800800)
  • National Natural Science Foundation of China

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