Interleukin‐23 regulates interleukin‐17 expression in wounds, and its inhibition accelerates diabetic wound healing through the alteration of macrophage polarization

Lee, James; Rodero, Mathieu P; Patel, Jatin; Moi, Davide; Mazzieri, Roberta; Khosrotehrani, Kiarash

doi:10.1096/fj.201700773r

Cited by 53 publications

(39 citation statements)

References 22 publications

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“…In obese diabetic mice, treatment with anti-IL-17A and anti-IL-23 antibodies improved wound re-epithelialization. In the same study, local wound IL-17A levels were lower in IL-23 deficient animals [77].…”

Section: The Th17/il-17a Axis In Diabetic Complicationsmentioning

confidence: 67%

Could IL-17A Be a Novel Therapeutic Target in Diabetic Nephropathy?

Lavoz

Rayego‐Mateos

Orejudo

et al. 2020

JCM

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Chronic kidney disease has become a major medical issue in recent years due to its high prevalence worldwide, its association with premature mortality, and its social and economic implications. A number of patients gradually progress to end-stage renal disease (ESRD), requiring then dialysis and kidney transplantation. Currently, approximately 40% of patients with diabetes develop kidney disease, making it the most prevalent cause of ESRD. Thus, more effective therapies for diabetic nephropathy are needed. In preclinical studies of diabetes, anti-inflammatory therapeutic strategies have been used to protect the kidneys. Recent evidence supports that immune cells play an active role in the pathogenesis of diabetic nephropathy. Th17 immune cells and their effector cytokine IL-17A have recently emerged as promising targets in several clinical conditions, including renal diseases. Here, we review current knowledge regarding the involvement of Th17/IL-17A in the genesis of diabetic renal injury, as well as the rationale behind targeting IL-17A as an additional therapy in patients with diabetic nephropathy.

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Section: The Th17/il-17a Axis In Diabetic Complicationsmentioning

confidence: 67%

Could IL-17A Be a Novel Therapeutic Target in Diabetic Nephropathy?

Lavoz

Rayego‐Mateos

Orejudo

et al. 2020

JCM

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“…Mice were wounded as per previous literature [ 28 ]. Mice were shaved and had Veet depilatory cream applied to remove excess hair.…”

Section: Methodsmentioning

confidence: 99%

The Small Molecule NLRP3 Inflammasome Inhibitor MCC950 Does Not Alter Wound Healing in Obese Mice

Lee

Robertson

Cooper

et al. 2018

IJMS

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The incidence of chronic wounds is escalating, and the associated healing process is especially problematic in an aging population with increased morbidity. Targeting increased inflammation in chronic wounds is a promising but challenging therapeutic strategy. Indeed, inflammation and especially macrophages are required for wound healing. As the NLRP3 inflammasome has been implicated with various other inflammatory diseases, in this study, we used MCC950—a selective NLRP3 small molecule inhibitor—on murine models of both acute and chronic wounds. This molecule, while tested for other inflammatory conditions, has never been investigated to reduce topical inflammation driving chronic wounds. We found that there were no significant differences when the treatment was applied either topically or orally in wild-type C57Bl/6 mice and that it even impaired wound healing in obese mice. The treatment was also unable to improve re-epithelialisation or angiogenesis, which are both required for the closure of wounds. We are inclined to believe that MCC950 may inhibit the closure of chronic wounds and that it does not alter wound-associated macrophage polarisation.

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“…Anti-IL-17A antibodies strengthen re-epithelialization of wounds in obese diabetic mice by altering the proportion of M1/M2 macrophage populations without any effect on scarring or fibrosis [63]. Local application of recombinant IL-17A leads to delayed wound healing and accelerated neutrophil accumulation in mice [64].…”

Section: Therapeutic Strategies Targeting Epidermal Scs and Relevant mentioning

confidence: 99%

Proinflammatory cytokines regulate epidermal stem cells in wound epithelialization

et al. 2020

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The skin, which serves as the first barrier of the human body, is particularly susceptible to exogenous injuries. Skin wounds, including acute burns and chronic non-healing ulcers, are commonly observed in clinics. Healing of skin wounds is a complex process, consisting of infiltration of inflammatory cells, cellular proliferation, and tissue remodeling phases, which restore the integrity and functions of the skin. Epithelialization is involved in wound healing through re-establishing an intact keratinocyte layer. Epidermal stem cells are indispensable for epithelialization, and they are regulated by multiple proinflammatory cytokines or growth factors. In this review, we summarize recent advances in the effect of these cytokines on migration, proliferation, and differentiation processes of epidermal stem cells. We also introduce promising therapeutic strategies targeting epidermal stem cells or related proinflammatory cytokines for patients with skin wounds.

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Interleukin‐23 regulates interleukin‐17 expression in wounds, and its inhibition accelerates diabetic wound healing through the alteration of macrophage polarization

Cited by 53 publications

References 22 publications

Could IL-17A Be a Novel Therapeutic Target in Diabetic Nephropathy?

Could IL-17A Be a Novel Therapeutic Target in Diabetic Nephropathy?

The Small Molecule NLRP3 Inflammasome Inhibitor MCC950 Does Not Alter Wound Healing in Obese Mice

Proinflammatory cytokines regulate epidermal stem cells in wound epithelialization

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