Reduced intraepidermal nerve fibre density in lesional and nonlesional prurigo nodularis skin as a potential sign of subclinical cutaneous neuropathy

Schuhknecht, B.; Marziniak, Martin; Wissel, A.; Phan, Ngoc Quan; Pappai, D.; Dangelmaier, J.; Metze, Dieter; Ständer, Sonja

doi:10.1111/j.1365-2133.2011.10306.x

Cited by 117 publications

(88 citation statements)

References 43 publications

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“…1b), although the increases of nerve density in patients with pruigo nodularis and psoriasis remain unclear. [10][11][12] Similar findings have been observed in animal models, such as nc/nga mice, a model of atopic dermatitis model, 13,14) and in dry skin model mice. 15,16) Such increases in nerve density are also found in the dermis of patients with atopic dermatitis and psoriasis.…”

Section: Histology Of Cutaneous Nerve Fibers In Atopic Dermatitissupporting

confidence: 67%

An Update on Peripheral Mechanisms and Treatments of Itch

Tominaga

Takamori

2013

Biological & Pharmaceutical Bulletin

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Histamine H 1 -receptor blockers are used to treat all types of itch resulting from serious skin diseases such as atopic dermatitis, as well as from renal and liver diseases. However, they often lack efficacy in chronic itch, a profound clinical problem that decreases quality of life. The development of effective treatments requires a full understanding of the fundamental mechanisms of itch. Recent studies have indicated that the pathogenic mechanisms of itch also involve agonists other than histamine, including proteases, neuropeptides, cytokines, and opioids, as well as their cognate receptors. Release of these pruritogenic mediators and modulators into the periphery may directly activate itch-mediating C-fibers via specific receptors on the nerve terminals. Histological observations have shown increased epidermal nerve densities in patients with atopic dermatitis, suggesting that the higher density is at least partly responsible for itch sensitization. This

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Section: Histology Of Cutaneous Nerve Fibers In Atopic Dermatitissupporting

confidence: 67%

An Update on Peripheral Mechanisms and Treatments of Itch

Tominaga

Takamori

2013

Biological & Pharmaceutical Bulletin

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“…In addition, it was intriguing to note that intraepidermal nerve fiber sprouting was most marked at the periphery, rather than at the center, of nodules. In human prurigo lesions, contradictory results were reported regarding nerve fiber innervation in the epidermis (33,44). These inconsistent results may be explained by the present mouse model demonstrating transitional changes in the intraepidermal nerve fiber density within lesions.…”

Section: Discussioncontrasting

confidence: 50%

Protective Role of STAT6 in Basophil-Dependent Prurigo-like Allergic Skin Inflammation

Hashimoto

Satoh

Yokozeki

2015

The Journal of Immunology

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Prurigo is a common, but treatment-resistant, skin disease characterized by persistent papules/nodules and severe itching. Prurigo occurs in association with various underlying diseases, such as diabetes, chronic renal failure, and internal malignancies. Atopic dermatitis is occasionally complicated by prurigo lesions. However, the pathology of prurigo is completely undefined. We demonstrate that repeated intradermal administration of Ag to IgE-transgenic mice causes persistent and pruritic papulonodular skin lesions mimicking prurigo. Skin lesions were histopathologically characterized by irregular acanthosis and dermal cellular infiltrates comprising eosinophils, mononuclear cells, and basophils, with epidermal nerve fiber sprouting. In vivo depletion of basophils alleviated skin reactions, indicating that the inflammation is basophil dependent. Unexpectedly, STAT6 signaling was unnecessary for skin lesion development if IgE was present. Moreover, the absence of STAT6 signaling exacerbated the inflammation, apparently as the result of impaired generation of an M2-type anti-inflammatory macrophage response. These results provide novel insights into the pathologic mechanisms underlying prurigo. Although basophils are indispensable for prurigo-like inflammation, Th2 immunity mediated by STAT6 appears to play a protective role, and therapies targeting Th2-type cytokines may risk aggravating the inflammation.

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“…Recently, it was reported that lesional and uninvolved PN skin biopsies showed significantly decreased intraepidermal nerve fiber density regardless of patient age, origin of PN, intensity or quality of pruritus. 3 However, our data showed nerve fiber elongation in epidermis of PN. This discrepancy may be explained by the difference in different sampling standards and immunostaining methods.…”

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confidence: 58%