Neuromodulatory treatment of recalcitrant plaque psoriasis with onabotulinumtoxinA

Aschenbeck, Kelly A.; Hordinsky, Maria; Kennedy, William R.; Wendelschafer‐Crabb, Gwen; Ericson, Marna E.; Kavand, Sima; Bertin, Ana Carina Junqueira; Dykstra, Dennis D.; Panoutsopoulou, Ioanna G.

doi:10.1016/j.jaad.2018.07.058

Cited by 25 publications

(26 citation statements)

References 5 publications

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“…However, this study was focused more on abnormal neurotransmitters secreted by skin nerve fibers because a number of studies showed that neurotransmitters might be important contributors to psoriasis and potential targets for future therapies 14,16,31 . Therefore, the expression levels of some neurotransmitters, such as SP, NKA, CGRP, and NPY, were examined.…”

Section: Discussionmentioning

confidence: 99%

Stress aggravates and prolongs imiquimod-induced psoriasis-like epidermal hyperplasis and IL-1β/IL-23p40 production

Wang

Zhang

et al. 2020

Journal of Leukocyte Biology

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Psoriasis is a common, chronic multifactorial inflammatory skin disease with both genetic and environmental components. A number of studies have suggested that psoriasis episodes are often preceded by stressful life events. Nevertheless, the underline mechanisms of stress in psoriasis remain unexplored. To address this question, we established an emotional stress mouse model induced by empty bottle stimulation, and applied imiquimod (IMQ), a ligand of TLR7/8 and effective potent immune activator, on the dorsal skin to induce psoriasis‐like lesions. We found that empty bottles induced emotional stress exaggerated and prolonged psoriasiform dermatitis, which appeared as more prominent epidermal hyperplasia in the emotional stress mice compared with the control mice. Higher mRNA expression of Il‐1β, Il‐17a, and Il‐22, as well as higher secretion of IL‐1β, IL‐12p40, IL‐17, and IL‐22 were observed in the skin lesion of emotional stress mice. The emotional stress condition and IMQ treatment synergistically led to higher expression levels of neurotransmitters and their receptors in the skin, especially substance P (SP), we also found that SP could stimulate DCs to secrete more IL‐23p40 in vitro. In addition, NK‐1R antagonist partially abrogated enhanced epidermal thickness and the level of neurotransmitters in emotional stress mice. Taken together, these results indicate that stress exacerbates and prolongs psoriasiform dermatitis in mice by up‐regulating IL‐1β and IL‐23p40, which were related to local DCs stimulated by abnormal SP.

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Section: Discussionmentioning

confidence: 99%

Stress aggravates and prolongs imiquimod-induced psoriasis-like epidermal hyperplasis and IL-1β/IL-23p40 production

Wang

Zhang

et al. 2020

Journal of Leukocyte Biology

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“…Recent case reports on the positive effect of BoNT-A injections in patients with psoriasis have promoted this pilot study to prove the hypothesis that BoNTs are effective in psoriasis. 7 This is a descriptive cross-sectional study with eight patients. The primary objective of the study is to evaluate the effect of BoNT-A on the change of total clinical score (TCS: sum of erythema 0-3, desquamation 0-3 and infiltration 0-3, range 0-9) of skin lesions of patient with plaque psoriasis at week 4.…”

Section: Introductionmentioning

confidence: 99%

Breaking paradigms in the treatment of psoriasis: Use of botulinum toxin for the treatment of plaque psoriasis

González

Franco

Londoño

et al. 2020

Dermatologic Therapy

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Some studies have demonstrated that neurotransmitters are involved in the pathogenesis of numerous skin conditions, including psoriasis, addressing the close correlation between the skin and the central nervous system. There are reports showing psoriasis improvement after peripheral nervous system injury. In addition, botulinum toxin has been reported as a treatment for several diseases, including psoriasis. This is a proof-of-concept study of botulinum toxin and psoriasis, involving eight patients with stable and recalcitrant plaques of psoriasis vulgaris. The lesions were 5 cm 2 at

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“…23,29 (5) Several tentative therapies, including dermatiome-shaving, capsaicin cream, resiniferatoxin, onabotulinumtoxinA, and K252a (a higha nity nerve growth factor receptor blocker), can improve psoriasis or psoriasiform dermatitis, through reducing lesional nerve bers or sensory denervation. [30][31][32][33][34][35][36] And nerve blockade based on locoregional anaesthesia has been proposed in psoriasis treatment. 37,38 (6) Sporadic case reports of psoriasis spared or alleviated in the site of nerve injured (e.g.…”

Section: Discussionmentioning

confidence: 99%

The nerve injuries interfere with the development of psoriasis

Qin

Sun

Chen

et al. 2020

Preprint

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BackgroundThe involvement of the nerve in psoriasis development has been suggested by sporadic case or case serial reports.ObjectivesTo provide multiple evidence for the nerve in psoriasis development with a retrospective case review, a literature review and a mouse-based experimental study.MethodsPsoriatic patients who had concomitant nerve injuries and such cases from the literatures were reviewed. And, on wild-type mouse level, unilateral denervation surgery was performed on the dorsal skin before and after the induction of psoriasiform dermatitis, respectively. Lesion visual scores were calculated, and lesion biopsies were taken for hematoxylin-eosin (HE) staining, immunofluorescence analysis, and RNA sequencing & bioinformatics analysis at the time before denervation surgery and the 2nd, 4th, 6th, 8th day after the surgery. ResultsAll clincal cases (20/20) showed that local lesions under the control of injured nerves relieved spontaneously or even cleared/spared, and only about 1/3 experienced partial recurrence. Next, experimental study based on mouse model demonstrated that the unilateral denervation prior to imiquimod application interfered with the enhancement of inflammatory reactions (e.g. adaptive immune response and Th17 cell differentiation pathway) and the induction of ipsilateral psoriasiform dermatitis. On the other hand, the unilateral denervation after the induction of psoriasiform dermatitis promoted the regression of inflammatory reactions (e.g. T cell activation, TNF signaling, and Th17 cell differentiation pathway) and the recovery of ipsilateral dermatitis. ConclusionOur study based on both retrospective clinical case review and wild-type mouse experiments provides multiple evidence for the involvement of the nerve in psoriasis development. Regulation of immune events, including TNF signaling and Th17 cell differentiation, may be one of the mechanisms of the nerve in psoriasis.

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Neuromodulatory treatment of recalcitrant plaque psoriasis with onabotulinumtoxinA

Cited by 25 publications

References 5 publications

Stress aggravates and prolongs imiquimod-induced psoriasis-like epidermal hyperplasis and IL-1β/IL-23p40 production

Stress aggravates and prolongs imiquimod-induced psoriasis-like epidermal hyperplasis and IL-1β/IL-23p40 production

Breaking paradigms in the treatment of psoriasis: Use of botulinum toxin for the treatment of plaque psoriasis

The nerve injuries interfere with the development of psoriasis

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