Role of nutritional intervention in negative pressure wound therapy (NPWT). Case report of patient treated by 'open abdomen' method.

Introduction Wound healing process depends on many factors. As it has been proved many times before, nutrition is one of the key factors in wound healing therapy. When there is an insufficient supply of nutrients and malnutrition, wound healing processes slow down and the inflammatory phase is prolonged, which requires high energy expenditure and as a consequence may lead to the loss of lean body mass and the development of sarcopenia and cachexia. This promotes the formation of non-healing chronic wounds. In this paper, we would like to emphasize the role of nutrition, as an integral part of wound healing processes, which should encompass the current metabolic needs associated with patient’s clinical condition. This case describes a young male patient with gastrointestinal tract insufficiency and an extensive postoperative wound treated by the open abdomen method. In the course of increased catabolism, water and electrolyte loss and disturbances as well as nutritional insufficiencies, body mass loss and progressive cachexia occurred in this patient and, as a consequence, the wound healing processes was significantly diminished. Inducing and maintaining the anabolic processes in the organism and control of the enhanced catabolism in response to metabolic stress or injury are essential actions in optimizing the treatment and healing process. These are possible to achieve by the early introduction of balanced and individualized nutritional treatment regimens, provision of the energy and appropriate nutrients, which enables the restoration of lean body mass and stimulation of the healing processes.

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The Insights of Microbes’ Roles in Wound Healing: A Comprehensive Review

Pharmaceutics ◽

10.3390/pharmaceutics13070981 ◽

2021 ◽

Vol 13 (7) ◽

pp. 981

Author(s):

Thambirajoo Maheswary ◽

Asma Abdullah Nurul ◽

Mh Busra Fauzi

Keyword(s):

Wound Healing ◽

Human Skin ◽

Chronic Wounds ◽

Healing Process ◽

Wound Dressings ◽

Normal Flora ◽

Chronic Injury ◽

Diverse Range ◽

Inflammatory Phase

A diverse range of normal flora populates the human skin and numbers are relatively different between individuals and parts of the skin. Humans and normal flora have formed a symbiotic relationship over a period of time. With numerous disease processes, the interaction between the host and normal flora can be interrupted. Unlike normal wound healing, which is complex and crucial to sustaining the skin’s physical barrier, chronic wounds, especially in diabetes, are wounds that fail to heal in a timely manner. The conditions become favorable for microbes to colonize and establish infections within the skin. These include secretions of various kinds of molecules, substances or even trigger the immune system to attack other cells required for wound healing. Additionally, the healing process can be slowed down by prolonging the inflammatory phase and delaying the wound repair process, which causes further destruction to the tissue. Antibiotics and wound dressings become the targeted therapy to treat chronic wounds. Though healing rates are improved, prolonged usage of these treatments could become ineffective or microbes may become resistant to the treatments. Considering all these factors, more studies are needed to comprehensively elucidate the role of human skin normal flora at the cellular and molecular level in a chronic injury. This article will review wound healing physiology and discuss the role of normal flora in the skin and chronic wounds.

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THE USE OF CHITIN AND CHITOSAN IN MANUFACTURING DRESSING MATERIALS

Progress on Chemistry and application of Chitin and its Derivatives ◽

10.15259/pcacd.25.002 ◽

2020 ◽

Vol XXV ◽

pp. 16-36

Author(s):

Ilona Latańska ◽

Beata Kolesińska ◽

Zbigniew Draczyński ◽

Witold Sujka

Keyword(s):

Wound Healing ◽

Medical Device ◽

Chronic Wounds ◽

Raw Materials ◽

Healing Process ◽

Accelerate Wound Healing ◽

Continuous Progress ◽

Chitin And Chitosan ◽

Dressing Materials ◽

Healing Processes

Despite continuous progress in the development of advanced dressing materials, there is a constant need for dressings used in an environment of infected and hard-to-heal wounds. Dressings that meet the above described requirements are products based on chitin and its derivatives. Chitosan and chitin derivative dressings are now becoming a very effective medical device in healing hard-to-heal wounds, as well as in the control of severely bleeding wounds. Chitosan and chitin are particularly valuable raw materials that accelerate wound healing processes, and they are also biocompatible and antibacterial. Dressings made of butyric-acetic chitin copolyester are intended for treating wounds of various aetiologies, including chronic wounds in which the healing process is disturbed by concomitant diseases. Materials based on chitosan are also widely used in the area of heavily bleeding and chronic wounds.

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Immunology of Acute and Chronic Wound Healing

Biomolecules ◽

10.3390/biom11050700 ◽

2021 ◽

Vol 11 (5) ◽

pp. 700

Author(s):

Kamila Raziyeva ◽

Yevgeniy Kim ◽

Zharylkasyn Zharkinbekov ◽

Kuat Kassymbek ◽

Shiro Jimi ◽

...

Keyword(s):

Wound Healing ◽

Chronic Wounds ◽

Chronic Wound ◽

Healing Process ◽

Inflammatory Factors ◽

Wound Healing Process ◽

Macrophage Phenotype ◽

Microbial Biofilms ◽

Inflammatory Phase ◽

Persistent Inflammation

Skin wounds greatly affect the global healthcare system, creating a substantial burden on the economy and society. Moreover, the situation is exacerbated by low healing rates, which in fact are overestimated in reports. Cutaneous wounds are generally classified into acute and chronic. The immune response plays an important role during acute wound healing. The activation of immune cells and factors initiate the inflammatory process, facilitate wound cleansing and promote subsequent tissue healing. However, dysregulation of the immune system during the wound healing process leads to persistent inflammation and delayed healing, which ultimately result in chronic wounds. The microenvironment of a chronic wound is characterized by high quantities of pro-inflammatory macrophages, overexpression of inflammatory mediators such as TNF-α and IL-1β, increased activity of matrix metalloproteinases and abundance of reactive oxygen species. Moreover, chronic wounds are frequently complicated by bacterial biofilms, which perpetuate the inflammatory phase. Continuous inflammation and microbial biofilms make it very difficult for the chronic wounds to heal. In this review, we discuss the role of innate and adaptive immunity in the pathogenesis of acute and chronic wounds. Furthermore, we review the latest immunomodulatory therapeutic strategies, including modifying macrophage phenotype, regulating miRNA expression and targeting pro- and anti-inflammatory factors to improve wound healing.

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Similarities between Tumour Immune Response and Chronic Wound Microenvironment: Influence of Mesenchymal Stromal/Stem Cells

Journal of Immunology Research ◽

10.1155/2021/6649314 ◽

2021 ◽

Vol 2021 ◽

pp. 1-11

Author(s):

Kimberly Thando Peta ◽

Melvin Anyasi Ambele ◽

Michael Sean Pepper

Keyword(s):

Stem Cells ◽

Wound Healing ◽

Natural Killer Cells ◽

Natural Killer ◽

Treatment Option ◽

Chronic Wounds ◽

Killer Cells ◽

Inflammatory Phase ◽

Stromal Stem Cells

Tumours are characterized by a state of chronic inflammation and are regarded as wounds that never heal. Mesenchymal stromal/stem cells (MSCs) are being considered as a possible treatment option. While MSCs can regulate the immune system, migrate to sites of inflammation, and are naturally immune-privileged, there have been contradictory reports on the role of these cells in the tumour microenvironment (TME). Some studies have suggested that MSCs promote tumourigenesis while others have suggested the contrary. To better evaluate the role of MSCs in the TME, it may be helpful to understand the role of MSCs in chronic wounds. Here, we discuss the role of MSCs in chronic wounds and extrapolate this to the TME. Chronic wounds are stuck in the inflammatory phase of wound healing, while in the case of the TME, both the inflammatory and proliferative phases are exploited. MSCs in chronic wounds promote a switch in macrophage phenotype from proinflammatory (M1) to anti-inflammatory (M2), thereby suppressing T, B, and natural killer cells, consequently promoting wound healing. In the case of the TME, MSCs are reported to promote tumorigenesis by suppressing T, B, and natural killer cells in addition to dendritic cells, cytotoxic T cells, and Th1-associated cytokines, thereby promoting tumour growth. Some studies have however suggested that MSCs inhibit tumourigenesis, depending on the source of the MSCs and the specific mediators involved. Therefore, the role of MSCs in the TME appears to be complex and may result in variable outcomes. Compelling evidence to suggest that MSCs are an effective treatment option against tumour progression is lacking.

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Regulatory Role of Nrf2 Signaling Pathway in Wound Healing Process

Molecules ◽

10.3390/molecules26092424 ◽

2021 ◽

Vol 26 (9) ◽

pp. 2424

Author(s):

Ipek Süntar ◽

Sümeyra Çetinkaya ◽

Emiliano Panieri ◽

Sarmistha Saha ◽

Brigitta Buttari ◽

...

Keyword(s):

Wound Healing ◽

Signaling Pathway ◽

Bioactive Compounds ◽

Wound Repair ◽

Chronic Wounds ◽

Healing Process ◽

Wound Healing Process ◽

Related Factor ◽

Nrf2 Signaling Pathway

Wound healing involves a series of cellular events in damaged cells and tissues initiated with hemostasis and finally culminating with the formation of a fibrin clot. However, delay in the normal wound healing process during pathological conditions due to reactive oxygen species, inflammation and immune suppression at the wound site represents a medical challenge. So far, many therapeutic strategies have been developed to improve cellular homeostasis and chronic wounds in order to accelerate wound repair. In this context, the role of Nuclear factor erythroid 2-related factor 2 (Nrf2) during the wound healing process has been a stimulating research topic for therapeutic perspectives. Nrf2 is the main regulator of intracellular redox homeostasis. It increases cytoprotective gene expression and the antioxidant capacity of mammalian cells. It has been reported that some bioactive compounds attenuate cellular stress and thus accelerate cell proliferation, neovascularization and repair of damaged tissues by promoting Nrf2 activation. This review highlights the importance of the Nrf2 signaling pathway in wound healing strategies and the role of bioactive compounds that support wound repair through the modulation of this crucial transcription factor.

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Nanomaterials Versus The Microbial Compounds With Wound Healing Property

Frontiers in Nanotechnology ◽

10.3389/fnano.2020.584489 ◽

2021 ◽

Vol 2 ◽

Author(s):

Fatemeh Salimi ◽

Fatemeh Mohammadipanah

Keyword(s):

Wound Healing ◽

Iron Oxide ◽

Carbon Nanomaterials ◽

Chronic Wounds ◽

Healing Process ◽

Solid Lipid ◽

Inflammatory Phase ◽

Metal Metal ◽

Silver Nps ◽

Gold Nps

Age and diabetes related slow-healing or chronic wounds may result in morbidity and mortality through persistent biofilms infections and prolonged inflammatory phase. Nano-materials [metal/metal oxide NPs (39%), lipid vehicles (21%), polymer NPs (19%), ceramic nanoparticles (NPs) (14%), and carbon nanomaterials (NMs) (7%)] can be introduced as a possible next-generation therapy because of either their intrinsic wound healing activity or via carrying bioactive compounds including, antibiotics, antioxidants, growth factor or stem cell. The nanomaterials have been shown to implicate in all four stages of wound healing including hemostasis (polymer NPs, ceramic NPs, nanoceria-6.1%), inflammation (liposome/vesicles/solid lipid NPs/polymer NPs/ceramic NPs/silver NPs/gold NPs/nanoceria/fullerenes/carbon-based NPs-32.7%), proliferation (vesicles/liposome/solid lipid NPs/gold NPs/silver NPs/iron oxide NPs/ceramic NPs/copper NPs/self-assembling elastin-like NPs/nanoceria/micelle/dendrimers/polymer NPs-57.1%), remodeling (iron oxide NPs/nanoceria-4.1%). Natural compounds from alkaloids, flavonoids, retinoids, volatile oil, terpenes, carotenoids, or polyphenolic compounds with proven antioxidant, anti-inflammatory, immunomodulatory, or antimicrobial characteristics are also well known for their potential to accelerate the wound healing process. In the current paper, we survey the potential and properties of nanomaterials and microbial compounds in improving the process of wound and scar healing. Finally, we review the potential biocompounds for incorporation to nano-material in perspective to designate more effective or multivalent wound healing natural or nano-based drugs.

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Plasminogen is a critical regulator of cutaneous wound healing

Thrombosis and Haemostasis ◽

10.1160/th15-08-0653 ◽

2016 ◽

Vol 115 (05) ◽

pp. 1001-1009 ◽

Cited By ~ 22

Author(s):

Rima Sulniute ◽

Yue Shen ◽

Yong-Zhi Guo ◽

Mahsa Fallah ◽

Nina Ahlskog ◽

...

Keyword(s):

Wound Healing ◽

Chronic Wounds ◽

Healing Process ◽

Inflammatory Cells ◽

Wound Healing Process ◽

Tissue Remodelling ◽

Inflammatory Phase ◽

Human Plasminogen ◽

Supplementary Material ◽

Deficient Mice

SummaryWound healing is a complicated biological process that consist of partially overlapping inflammatory, proliferation and tissue remodelling phases. A successful wound healing depends on a proper activation and subsequent termination of the inflammatory phase. The failure to terminate the inflammation halts the completion of wound healing and is a known reason for formation of chronic wounds. Previous studies have shown that wound closure is delayed in plasminogendeficient mice, and a role for plasminogen in dissection of extracellular matrix was suggested. However, our finding that plasminogen is transported to the wound by inflammatory cells early during the healing process, where it potentiates inflammation, indicates that plasminogen may also have other roles in the wound healing process. Here we report that plasminogen-deficient mice have extensive fibrin and neutrophil depositions in the wounded area long after re-epithelialisation, indicating inefficient debridement and chronic inflammation. Delayed formation of granulation tissue suggests that fibroblast function is impaired in the absence of plasminogen. Therefore, in addition to its role in the activation of inflammation, plasminogen is also crucial for subsequent steps, including resolution of inflammation and activation of the proliferation phase. Importantly, supplementation of plasminogen-deficient mice with human plasminogen leads to a restored healing process that is comparable to that in wild-type mice. Besides of being an activator of the inflammatory phase during wound healing, plasminogen is also required for the subsequent termination of inflammation. Based on these results, we propose that plasminogen may be an important future therapeutic agent for wound treatment.Supplementary Material to this article is available online at www.thrombosis-online.com.

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The role of miRNAs in the inflammatory phase of skin wound healing

AIMS Allergy and Immunology ◽

10.3934/allergy.2021020 ◽

2021 ◽

Vol 5 (4) ◽

pp. 264-278

Author(s):

Federica Serra ◽

◽

Lisa Aielli ◽

Erica Costantini ◽

◽

...

Keyword(s):

Wound Healing ◽

Wound Repair ◽

Chronic Wounds ◽

Medical Problem ◽

Skin Wound ◽

Skin Wound Healing ◽

Damage Site ◽

Inflammatory Phase ◽

Peripheral Cells

<abstract> <p>Wound healing (WH) is a fundamental physiological process to keep the integrity of the skin, therefore impaired and chronic WH is a common and severe medical problem and represent one of the biggest challenges of public health. The resolution of the WH inflammatory phase is characterized by a complex series of events that involves many cellular types, especially neutrophils, macrophages and inflammatory mediators, which are crucial for a correct wound closure. MicroRNAs (miRNAs) play essential roles in wound repair. In fact, miR-142 is linked to inflammation modulating neutrophils' chemotaxis and polarization, while the polarization of M1 toward the M2 phenotype is driven by miR-223 and miR-132 is linked to chemokines and cytokines that activate endothelial cells and attract leukocytes and peripheral cells to the damage site. Thus, understanding the dysregulation of miRNAs in WH will be decisive for the development of new and more effective therapies for the management of chronic wounds.</p> </abstract>

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Inflammatory M1-like macrophages polarized by NK-4 undergo enhanced phenotypic switching to an anti-inflammatory M2-like phenotype upon co-culture with apoptotic cells

Journal of Inflammation ◽

10.1186/s12950-020-00267-z ◽

2021 ◽

Vol 18 (1) ◽

Author(s):

Keizo Kohno ◽

Satomi Koya-Miyata ◽

Akira Harashima ◽

Takahiko Tsukuda ◽

Masataka Katakami ◽

...

Keyword(s):

Wound Healing ◽

Chronic Wounds ◽

Macrophage Polarization ◽

Phenotypic Switching ◽

Apoptotic Cells ◽

Phenotypic Switch ◽

Inflammatory Phase ◽

M1 Macrophage ◽

Tnf Α ◽

Anti Inflammatory

Abstract Background NK-4 has been used to promote wound healing since the early-1950s; however, the mechanism of action of NK-4 is unknown. In this study, we examined whether NK-4 exerts a regulatory effect on macrophages, which play multiple roles during wound healing from the initial inflammatory phase until the tissue regeneration phase. Results NK-4 treatment of THP-1 macrophages induced morphological features characteristic of classically-activated M1 macrophages, an inflammatory cytokine profile, and increased expression of the M1 macrophage-associated molecules CD38 and CD86. Interestingly, NK-4 augmented TNF-α production by THP-1 macrophages in combination with LPS, Pam3CSK4, or poly(I:C). Furthermore, NK-4 treatment enhanced THP-1 macrophage phagocytosis of latex beads. These results indicate that NK-4 drives macrophage polarization toward an inflammatory M1-like phenotype with increased phagocytic activity. Efferocytosis is a crucial event for resolution of the inflammatory phase in wound healing. NK-4-treated THP-1 macrophages co-cultured with apoptotic Jurkat E6.1 (Apo-J) cells switched from an M1-like phenotype to an M2-like phenotype, as seen in the inverted ratio of TNF-α to IL-10 produced in response to LPS. We identified two separate mechanisms that are involved in this phenotypic switch. First, recognition of phosphatidylserine molecules on Apo-J cells by THP-1 macrophages downregulates TNF-α production. Second, phagocytosis of Apo-J cells by THP-1 macrophages and activation of PI3K/Akt signaling pathway upregulates IL-10 production. Conclusion It is postulated that the phenotypic switch from a proinflammatory M1-like phenotype to an anti-inflammatory M2-like phenotype is dysregulated due to impaired efferocytosis of apoptotic neutrophils at the wound site. Our results demonstrate that NK-4 improves phagocytosis of apoptotic cells, suggesting its potential as a therapeutic strategy to resolve sustained inflammation in chronic wounds.

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