Antipruritic Effects of Botulinum Neurotoxins

Gazerani, Parisa

doi:10.3390/toxins10040143

Cited by 17 publications

(15 citation statements)

References 124 publications

(164 reference statements)

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“…126,127 Injection of BTX at the site of localized pruritus has been reported to reduce localized itch in patients with conditions like brachioradial pruritus, notalgia paresthetica, and lichen simplex chronicus. 128 Pruritus normally returns within months of receiving botulinum toxin treatment, and desensitization can occur with repeated treatments. 128…”

Section: Botulinum Toxinmentioning

confidence: 99%

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Itch: From mechanism to (novel) therapeutic approaches

Yosipovitch

Rosen

Hashimoto

2018

Journal of Allergy and Clinical Immunology

260

307

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Itch is a common sensory experience that is prevalent in patients with inflammatory skin diseases, as well as in those with systemic and neuropathic conditions. In patients with these conditions, itch is often severe and significantly affects quality of life. Itch is encoded by 2 major neuronal pathways: histaminergic (in acute itch) and nonhistaminergic (in chronic itch). In the majority of cases, crosstalk existing between keratinocytes, the immune system, and nonhistaminergic sensory nerves is responsible for the pathophysiology of chronic itch. This review provides an overview of the current understanding of the molecular, neural, and immune mechanisms of itch: beginning in the skin, proceeding to the spinal cord, and eventually ascending to the brain, where itch is processed. A growing understanding of the mechanisms of chronic itch is expanding, as is our pipeline of more targeted topical and systemic therapies. Our therapeutic armamentarium for treating chronic itch has expanded in the last 5 years, with developments of topical and systemic treatments targeting the neural and immune systems.

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Section: Botulinum Toxinmentioning

confidence: 99%

“…128 Pruritus normally returns within months of receiving botulinum toxin treatment, and desensitization can occur with repeated treatments. 128…”

Section: Botulinum Toxinmentioning

confidence: 99%

Itch: From mechanism to (novel) therapeutic approaches

Yosipovitch

Rosen

Hashimoto

2018

Journal of Allergy and Clinical Immunology

260

307

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“…inactivate VAMPs. Thus, attenuation of TRPA1 and TRPV1 expression and their surface trafficking, plus inhibition of itchrelated neuropeptide release from pruritic nerve would underlie the observed anti-pruritic activity of BoNTs in animal models of chronic itch and in patients with itch conditions (171,174).…”

Section: Future Therapeutic Against Potentiation Of Trp Channelsmentioning

confidence: 99%

Th2 Modulation of Transient Receptor Potential Channels: An Unmet Therapeutic Intervention for Atopic Dermatitis

Meng

Fischer

et al. 2021

Front. Immunol.

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Atopic dermatitis (AD) is a multifaceted, chronic relapsing inflammatory skin disease that affects people of all ages. It is characterized by chronic eczema, constant pruritus, and severe discomfort. AD often progresses from mild annoyance to intractable pruritic inflammatory lesions associated with exacerbated skin sensitivity. The T helper-2 (Th2) response is mainly linked to the acute and subacute phase, whereas Th1 response has been associated in addition with the chronic phase. IL-17, IL-22, TSLP, and IL-31 also play a role in AD. Transient receptor potential (TRP) cation channels play a significant role in neuroinflammation, itch and pain, indicating neuroimmune circuits in AD. However, the Th2-driven cutaneous sensitization of TRP channels is underappreciated. Emerging findings suggest that critical Th2-related cytokines cause potentiation of TRP channels, thereby exaggerating inflammation and itch sensation. Evidence involves the following: (i) IL-13 enhances TRPV1 and TRPA1 transcription levels; (ii) IL-31 sensitizes TRPV1 via transcriptional and channel modulation, and indirectly modulates TRPV3 in keratinocytes; (iii) The Th2-cytokine TSLP increases TRPA1 synthesis in sensory neurons. These changes could be further enhanced by other Th2 cytokines, including IL-4, IL-25, and IL-33, which are inducers for IL-13, IL-31, or TSLP in skin. Taken together, this review highlights that Th2 cytokines potentiate TRP channels through diverse mechanisms under different inflammatory and pruritic conditions, and link this effect to distinct signaling cascades in AD. This review strengthens the notion that interrupting Th2-driven modulation of TRP channels will inhibit transition from acute to chronic AD, thereby aiding the development of effective therapeutics and treatment optimization.

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“…The histamine acts as the main mediator of H1-H4 receptors, responsible for activation of the target molecules within the sensory neurons that code pruritic signals. BoNTA also downregulates transient receptor potential channel type V1 (TRPV1) and type A (TRPA1), responsible for histamine-mediated and non-histamine-dependent itch, respectively [8].…”

Section: Effects Of Bonta On the Inflammatory Cascadementioning

confidence: 99%

Treatment of Immature Scars with Botulinum Toxin

Chambers¹

2020

Textbook on Scar Management

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Using Botulinum neurotoxin type A (BoNTA) has yielded promising results in the treatment of immature scars. The biological effects of the toxin on tissue healing appear to be complex and multidimensional and still require additional research. Nevertheless, it is clear that not only does BoNTA reduce muscle tension at the edges of wounds, but it also provides anti-inflammatory effects, promotes angiogenesis and healing, and exerts mediatory or inhibitory effects on a variety of cells. In clinical practice, this pluripotency of BoNTA has been recognized as a therapeutic choice for both prophylaxis and treatment of excessive scarring.

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Antipruritic Effects of Botulinum Neurotoxins

Cited by 17 publications

References 124 publications

Itch: From mechanism to (novel) therapeutic approaches

Itch: From mechanism to (novel) therapeutic approaches

Th2 Modulation of Transient Receptor Potential Channels: An Unmet Therapeutic Intervention for Atopic Dermatitis

Treatment of Immature Scars with Botulinum Toxin

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