Emerging drugs for the treatment of chronic pruritic diseases

Fourzali, Kayla; Golpanian, Rachel Shireen; Yosipovitch, Gil

doi:10.1080/14728214.2020.1801632

Cited by 9 publications

(9 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Currently available data suggest that in AD, itching is a result of inflammation. However, this conclusion may not be generalized for a number of itchy skin disorders such as prurigo nodularis in which targeting itch remains promising 193,205,[210][211][212] .…”

Section: Targeting the Key Symptom: Itch-scratch Cyclementioning

confidence: 95%

Atopic dermatitis: an expanding therapeutic pipeline for a complex disease

Bieber

2021

Nat Rev Drug Discov

326

294

View full text Add to dashboard Cite

show abstract

Section: Targeting the Key Symptom: Itch-scratch Cyclementioning

confidence: 95%

Atopic dermatitis: an expanding therapeutic pipeline for a complex disease

Bieber

2021

Nat Rev Drug Discov

326

294

View full text Add to dashboard Cite

show abstract

“…Irrespective of the original cause and underlying pathophysiology, chronic pruritic conditions determine profound suffering of the affected individuals on multiple dimensions, with significant emotional-psychological burden, sleep interference, work impairment, and loss of productivity [45]. In the next section, we describe the role of type-2 inflammation as the main driver of pruritus associated with both communicable and non-communicable skin conditions, briefly pointing at therapeutic-translational aspects (summarized in Table 3) [46].…”

Section: The Top Itchy Skin Diseasesmentioning

confidence: 99%

Pruritus as a Distinctive Feature of Type 2 Inflammation

et al. 2021

Self Cite

View full text Add to dashboard Cite

Pruritus is a common symptom of several skin diseases, both inflammatory and neoplastic. Pruritus might have a tremendous impact on patients’ quality of life and strongly interfere with sleep, social, and work activities. We review the role of type-2 inflammation and immunity in the pathogenesis of chronic pruritic conditions of the skin. Type 2 cytokines, including IL-4, IL-13, thymic stromal lymphopoietin, periostin, IL-31, IL-25, and IL-33 are released by mast cells, innate lymphoid cells 2, keratinocytes, and type 2 T lymphocytes, and are master regulators of chronic itch. These cytokines might act as direct pruritogen on primary sensory neurons (pruriceptors) or alter the sensitivity to other itch mediators Type 2 inflammation- and immunity-dominated skin diseases, including atopic dermatitis, prurigo nodularis, bullous pemphigoid, scabies, parasitic diseases, urticaria, and Sézary syndrome are indeed conditions associated with most severe pruritus. In contrast, in other skin diseases, such as scleroderma, lupus erythematosus, hidradenitis suppurativa, and acne, type 2 inflammation is less represented, and pruritus is milder or variable. Th2 inflammation and immunity evolved to protect against parasites, and thus, the scratching response evoked by pruritus might have developed to alert about the presence and to remove parasites from the skin surface.

show abstract

“…The possible targets can be the pruritic mediators, their receptors and the related signaling pathways carefully chosen in light of the underlying pathology. The putative efficiency of such a selective approach is supported by several successful attempts using monoclonal neutralizing antibodies targeting T h 2 and T h 17 cytokines or their receptors e.g., in the treatment of AD and psoriasis, respectively ( Fourzali et al, 2020 ; Zhang and He, 2020 ; Garcovich et al, 2021 ). The related signal transduction of these receptors can also be successfully targeted e.g., by JAK or phosphodiesterase 4 inhibitors ( Fourzali et al, 2020 ; Soeberdt et al, 2020 ).…”

Section: Therapeutic Conclusionmentioning

confidence: 99%

“…The putative efficiency of such a selective approach is supported by several successful attempts using monoclonal neutralizing antibodies targeting T h 2 and T h 17 cytokines or their receptors e.g., in the treatment of AD and psoriasis, respectively ( Fourzali et al, 2020 ; Zhang and He, 2020 ; Garcovich et al, 2021 ). The related signal transduction of these receptors can also be successfully targeted e.g., by JAK or phosphodiesterase 4 inhibitors ( Fourzali et al, 2020 ; Soeberdt et al, 2020 ). Future alternative targets may be neural receptors (e.g., MRGPRs), signaling molecules, and ion channels (e.g., TRP channels) involved in the transduction of itch ( Buddenkotte and Steinhoff, 2010 ; Tóth et al, 2015 ; Moore et al, 2018 ; Xie and Hu, 2018 ; Golpanian and Yosipovitch, 2020 ).…”

Section: Therapeutic Conclusionmentioning

confidence: 99%

Pruritus: A Sensory Symptom Generated in Cutaneous Immuno-Neuronal Crosstalk

et al. 2022

View full text Add to dashboard Cite

Pruritus or itch generated in the skin is one of the most widespread symptoms associated with various dermatological and systemic (immunological) conditions. Although many details about the molecular mechanisms of the development of both acute and chronic itch were uncovered in the last 2 decades, our understanding is still incomplete and the clinical management of pruritic conditions is one of the biggest challenges in daily dermatological practice. Recent research revealed molecular interactions between pruriceptive sensory neurons and surrounding cutaneous cell types including keratinocytes, as well as resident and transient cells of innate and adaptive immunity. Especially in inflammatory conditions, these cutaneous cells can produce various mediators, which can contribute to the excitation of pruriceptive sensory fibers resulting in itch sensation. There also exists significant communication in the opposite direction: sensory neurons can release mediators that maintain an inflamed, pruritic tissue-environment. In this review, we summarize the current knowledge about the sensory transduction of pruritus detailing the local intercellular interactions that generate itch. We especially emphasize the role of various pruritic mediators in the bidirectional crosstalk between cutaneous non-neuronal cells and sensory fibers. We also list various dermatoses and immunological conditions associated with itch, and discuss the potential immune-neuronal interactions promoting the development of pruritus in the particular diseases. These data may unveil putative new targets for antipruritic pharmacological interventions.

show abstract

Emerging drugs for the treatment of chronic pruritic diseases

Cited by 9 publications

References 81 publications

Atopic dermatitis: an expanding therapeutic pipeline for a complex disease

Atopic dermatitis: an expanding therapeutic pipeline for a complex disease

Pruritus as a Distinctive Feature of Type 2 Inflammation

Pruritus: A Sensory Symptom Generated in Cutaneous Immuno-Neuronal Crosstalk

Contact Info

Product

Resources

About