Th2 cytokines enhance TrkA expression, upregulate proliferation, and downregulate differentiation of keratinocytes

Matsumura, Sayaka; Terao, Mineko; Murota, Hiroyuki; Katayama, Ichiro

doi:10.1016/j.jdermsci.2015.02.021

Cited by 33 publications

(34 citation statements)

References 31 publications

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“…NGF, which can be released from mast cells (Groneberg et al, 2005) and also by eosinophils (Kobayashi et al, 2002), leads to activation, sensitization and sprouting of skin nerves, as well as to proliferation and differentiation of keratinocytes. These observations may explain the dermal neuronal hyperplasia and hyperplasia of the epidermis (Matsumura et al, 2015). Topical NGF antagonists may be thus beneficial in treating PN, but have not been investigated in PN until now.…”

Section: What Does This Review Add?mentioning

confidence: 99%

The pathogenesis of Prurigo nodularis – ‘Super‐Itch’ in exploration

Zeidler

Ständer

2015

European Journal of Pain

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Prurigo nodularis (PN) is characterized by multiple hyperkeratotic nodules, papules and the presence of intensive pruritus. This leads to an impaired quality of life and high burden due not only to the severe itch but also the chronic, skin lesions and lack of treatment options. The pathogenesis of PN is not completely clarified. Previous studies have demonstrated just how important the interaction between cutaneous nerve fibres and immune cells is. Besides a reduced intraepidermal nerve fibre density, there are increased dermal levels of neuropeptides such as substance P, calcitonin gene-related peptide and nerve growth factor, as well as a predominant presence of eosinophils and mast cells. An interaction of these factors results in a complex relationship which will be discussed in this article.

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Section: What Does This Review Add?mentioning

confidence: 99%

The pathogenesis of Prurigo nodularis – ‘Super‐Itch’ in exploration

Zeidler

Ständer

2015

European Journal of Pain

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“…In the skin, the main producer of nerve growth factor are keratinocytes [107], although fibroblasts [108, 109] and endothelial cells [110, 111] have also been shown to synthesize and release nerve growth factor. Nerve growth factor receptors have been seen in the skin [112] as well as primary and secondary lymphoid organs [113, 114]. …”

Section: Nerve Growth Factormentioning

confidence: 99%

“…Additionally, elevated expression of nerve growth factor has been seen in peripheral blood eosinophils of human patients [121] and in the diseased epidermis and dermis in the NC/Nga mouse model of atopic dermatitis [122]. Also of note, the onset of the pruritic lesions of atopic dermatitis was associated with increased TrkA receptor (specific for nerve growth factor) expression on keratinocytes [112]. …”

Section: Nerve Growth Factormentioning

confidence: 99%

Immunoregulatory Effects of Neuropeptides on Endothelial Cells: Relevance to Dermatological Disorders

Mehta

Granstein²

2019

Dermatology

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Many skin diseases, including psoriasis and atopic dermatitis, have a neurogenic component. In this regard, bidirectional interactions between components of the nervous system and multiple target cells in the skin and elsewhere have been receiving increasing attention. Neuropeptides released by sensory nerves that innervate the skin can directly modulate functions of keratinocytes, Langerhans cells, dermal dendritic cells, mast cells, dermal microvascular endothelial cells and infiltrating immune cells. As a result, neuropeptides and neuropeptide receptors participate in a complex, interdependent network of mediators that modulate the skin immune system, skin inflammation, and wound healing. In this review, we will focus on recent studies demonstrating the roles of α-melanocyte-stimulating hormone, calcitonin gene-related peptide, substance P, somatostatin, vasoactive intestinal peptide, pituitary adenylate cyclase-activating peptide, and nerve growth factor in modulating inflammation and immunity in the skin through their effects on dermal microvascular endothelial cells.

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“…138 TRPV1 is mainly expressed in keratinocytes, nerve fibers, as well as mast cells. 138 TRPV1 is mainly expressed in keratinocytes, nerve fibers, as well as mast cells.…”

Section: Ion Channel Inhibitors and Potential Targeted Therapiesmentioning

confidence: 99%

Immune mediators and therapies for pruritus in atopic dermatitis and psoriasis

Zhou

et al. 2019

J Cutaneous Imm & Allergy

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractAtopic dermatitis (AD) and psoriasis (Pso) are two common inflammatory skin diseases which are symptomatically characterized by pruritus to variable degrees.Whereas AD is nearly always associated with pruritus, only 50%-70% of patients with Pso suffer from itching. Within the last decade, the development of biologic agents targeting specific cytokines or cytokine receptors has led to tremendous progress in suppressing inflammation (and thus improving quality of life) in these two diseases.While suppressing inflammation would generally reduce pruritus in these inflammatory diseases, pruritus is still recalcitrant for treatment in some patients due to relative lack of therapeutics that specifically inhibit pruritus signaling. There is abundant evidence that certain cytokines and neuropeptides-ion channels signaling mediate pruritus that is independent of inflammation in AD and psoriasis. Of note, Janus kinase (JAK) and nerve growth factor (NGF)-tropomyosin receptor kinase A (TrkA)transient receptor potential vanilloid 1 (TRPV1) signaling partially regulates pruritus in AD and psoriasis. JAK kinases inhibitors decrease the extent of itch in patients with AD and psoriasis. In clinical trials, topical inhibitors of TrkA and TRPV1 have been reported to reduce pruritus in patients with Pso and AD, respectively. In this article, we review recent literature knowledge regarding the mechanisms underlying pruritus in AD and Pso, providing hypotheses for why pruritus may be more common in AD than in Pso. In light of the different mechanisms underlying these two diseases, the current and developing therapeutics, either in human clinical trials or animal studies, for targeting pruritus are also discussed. K E Y W O R D SIL-31, neuropeptide, PAR2, SP, thymic stromal lymphopoietin, TRPA1, TRPV1

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Th2 cytokines enhance TrkA expression, upregulate proliferation, and downregulate differentiation of keratinocytes

Cited by 33 publications

References 31 publications

The pathogenesis of Prurigo nodularis – ‘Super‐Itch’ in exploration

The pathogenesis of Prurigo nodularis – ‘Super‐Itch’ in exploration

Immunoregulatory Effects of Neuropeptides on Endothelial Cells: Relevance to Dermatological Disorders

Immune mediators and therapies for pruritus in atopic dermatitis and psoriasis

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