Psoriasis is a complex long-lasting inflammatory skin disease with high prevalence and associated comorbidity. It is characterized by epidermal hyperplasia and dermal infiltration of immune cells. Here, we review the role of keratinocytes in the pathogenesis of psoriasis, focusing on factors relevant to genetics, cytokines and receptors, metabolism, cell signaling, transcription factors, non-coding RNAs, antimicrobial peptides, and proteins with other different functions. The critical role of keratinocytes in initiating and maintaining the inflammatory state suggests the great significance of targeting keratinocytes for the treatment of psoriasis. 

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Advances in the pathogenesis of psoriasis: from keratinocyte perspective

Introduction: The heterogeneous pool of cells found in the stromal vascular fraction of adipose tissue (SVF) and the purified mesenchymal stromal/stem cells (ASCs) isolated from this pool have increasingly been used as therapeutic tools in regenerative medicine.Areas covered: As SVF and ASCs are different, and should be used in different manners according to various clinical and biological indications, we reviewed the current literature, and focused on the clinical use of SVF to appraise the main medical fields for development. Both enzymatic digestion and mechanical disruption have been used to obtain SVF for non-homologous use. The safety and/or benefits of SVF have been examined in 71 clinical studies in various contexts, mainly musculoskeletal conditions, wound healing, urogenital, and cardiovascular and respiratory diseases. The use of SVF as a therapy remains experimental, with few clinical trials.Expert opinion: SVF provides a cellular and molecular microenvironment for regulation of ASC' activities under different clinical conditions. SVF may enhance angiogenesis and neovascularization in wound healing, urogenital and cardiovascular diseases. In joint conditions, therapeutic benefits may rely on paracrine immune-modulatory and anti-inflammatory mechanisms. Novel point of care methods are emerging to refine SVF in ways that meet the regulatory requirements for minimal manipulation.

Stromal vascular fraction technologies and clinical applications

Chronic wounds are the result of disruptions in the body's usual process of healing. They are not only a source of significant pain and discomfort but also, more importantly, an unguarded port of entry for pathogens into the body. While our current understanding of this phenomenon is far from complete, findings in physiological patterns and advancements in wound healing technologies have helped develop wound management and healing solutions to this long-standing medical challenge. This review presents an overview of known wound healing mechanics, abnormalities that lead to chronic wounds, and a summary of established and new wound healing technologies. Various approaches to heal wounds are discussed, from dermal replacements to advanced biomaterial-based treatments, from cell-, synthetic-, and composite-based approaches to preclinical approaches, which make developing such products possible. While tested breakthrough products are described, the authors focused more on recently developed innovations, which are at varying stages of maturity. The review concludes with a note on future perspectives and opinions on where the field and industry are headed and where they should be. Impact Statement Wound healing is an important area of research and clinical practice, and has captured the attention of tissue engineers since the nascent beginnings of the discipline. Tissue-engineered skin was the first FDA-approved product, achieved in 1996. Despite this success, and the passage of time, healing wounds, particularly chronic wounds, remains a vexing challenge. This comprehensive review article will provide readers with a synopsis of current issues, research approaches, animal models, technologies, and products that span the continuum from early development to clinical studies, in the hope of fueling new interests and ideas to overcome this long-standing medical challenge.

Healing of Chronic Wounds: An Update of Recent Developments and Future Possibilities.

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Chronic ulcers remain a difficult challenge in healthcare systems. While treatment options are limited, stem cells may be a novel alternative. Adipose-derived stem cells (ADSC) have become increasingly popular compared with bone marrow-derived stem cells as they are far easier to harvest. To summarize the current status of treating chronic ulcers with ADSC, this systematic review includes all clinical trials on the subject from PubMed and EmBase, as well as all registered clinical trials on ClinicalTrials.Gov. A total of nine clinical trials and fourteen registered trials were included. The studies were significantly different in terms of study design and patient population, and the overall quality of the studies was low to moderate. Despite the overall low study quality and the significant differences between the studies, some conclusions were consistent: ADSCs are safe, improve the healing of chronic ulcers, and reduce pain. As these results are consistent despite the shortcomings of the studies, they appear to highlight the efficacy of ADSCs in the treatment of chronic ulcers. Larger numbers of higher quality studies are needed to determine the precise role of ADSCs in treating chronic leg ulcers.

/pdf/adipose-derived-stem-cells-for-treatment-of-chronic-ulcers-3f1o7m3mxp.pdf

Adipose-derived stem cells for treatment of chronic ulcers: current status

Background
The stromal vascular fraction (SVF) of adipose tissue consists of cellular subpopulations with distinct regenerative potential.

Objective
To investigate the regenerative capacities of autologous SVF cells in the treatment of chronic leg ulcers of venous (VLU) and arterial-venous (AVLU) origin.

Methods
Multimorbid ulcer patients received a singular topical treatment with 9–15 × 106 SVF cells, separated from abdominal lipoaspirates by digestion with collagenase and neutral protease and applied immediately after isolation. The primary endpoints were the change in wound size 12 weeks after treatment and evaluation of adverse events. Secondary endpoints included the time to complete wound epithelialization and change in pain levels. Postoperative wound treatment modalities and treatment of comorbidities were not intensified compared with pre-operative management. Follow-up period was at least 6 months.

Results
Sixteen elderly ulcer patients (seven with VLU, nine with AVLU) were treated as described. All VLU patients (median ulcer size: 48.25 cm2) and four of nine AVLU patients showed complete epithelialization of the ulcers within 71–174 days. In three patients with large ulcerations on both legs, ulcerations on the non-treated, contralateral leg also epithelialized. Patients reported a considerable rapid decrease in pain intensity by 2.5 points on average on a visual scale from 1 to 5 within the first 2 weeks after treatment. The patients were followed up for 9–44 months (median: 30 months). No severe side-effects were observed.

Conclusions
The use of SVF cells presents an effective, minimally invasive option for the treatment of VLU and AVLU even in multimorbid patients. In patients with larger predominantly ischaemic AVLU and comorbidities, one-time application of the used amounts of SVF cells was not sufficient in the majority of cases.

Therapy of ulcus cruris of venous and mixed venous arterial origin with autologous, adult, native progenitor cells from subcutaneous adipose tissue: a prospective clinical pilot study.

Background Key pathogenic events of psoriasis and atopic eczema (AE) are misguided immune reactions of the skin. IL-17C is an epithelial-derived cytokine, whose impact on skin inflammation is unclear. Objective We sought to characterize the role of IL-17C in human ISD. Methods IL-17C gene and protein expression was assessed by immunohistochemistry and transcriptome analysis. Primary human keratinocytes were stimulated and expression of cytokines chemokines was determined by qRT-PCR and luminex assay. Neutrophil migration towards supernatant of stimulated keratinocytes was assessed. IL-17C was depleted using a new IL-17C-specific antibody (MOR106) in murine models of psoriasis (IL-23 injection model) and AE (MC903 model) as well as in human skin biopsies of psoriasis and AE. Effects on cell influx (mouse models) and gene expression (human explant cultures) were determined. Results Expression of IL-17C mRNA and protein was elevated in various ISD. We demonstrate that IL-17C potentiates the expression of innate cytokines, antimicrobial peptides (IL-36G, S100A7 and HBD2) and chemokines (CXCL8, CXCL10, CCL5 and VEGF) and the autocrine induction of IL-17C in keratinocytes. Cell-free supernatant of keratinocytes stimulated with IL-17C was strongly chemotactic for neutrophils, thus demonstrating a critical role for IL-17C in immune cell recruitment. IL-17C depletion significantly reduced cell numbers of T cells, neutrophils and eosinophils in murine models of psoriasis and AE and led to a significant downregulation of inflammatory mediators in human skin biopsies of psoriasis and AE ex vivo. Conclusion IL-17C amplifies epithelial inflammation in Th2 and Th17 dominated skin inflammation and represents a promising target for the treatment of ISD.

IL‐17C amplifies epithelial inflammation in human psoriasis and atopic eczema

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Therapy of ulcus cruris of venous and mixed venous arterial origin with autologous, adult, native progenitor cells from subcutaneous adipose tissue: a prospective clinical pilot study.

IL‐17C amplifies epithelial inflammation in human psoriasis and atopic eczema