Periostin Activation of Integrin Receptors on Sensory Neurons Induces Allergic Itch

Mishra, Santosh K.; Wheeler, Joshua J.; Pitake, Saumitra; Ding, Huiping; Jiang, Changyu; Fukuyama, Tomoki; Paps, Judy S.; Ralph, P; Coyne, Jacob; Parkington, Michelle K.; DeBrecht, Jennifer; Ehrhardt-Humbert, Lauren; Cruse, Glenn; Bäumer, Wolfgang; Ji, Ru-Rong; Ko, Mei‐Chuan; Olivry, Thierry

doi:10.1016/j.celrep.2020.03.036

Cited by 80 publications

(78 citation statements)

References 99 publications

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“…Cathepsin S, another epidermal cystein protease, is involved in both AD-related inflammation and in histamine-independent itch, by activating Mas-related G-protein-coupled receptors (Mrgprs) and PAR-2 on sensory neurons [20,21]. Furthermore, the multifunctional ECM protein periostin can directly activate primary sensory afferents, via its aVβ3 integrin receptor, in the skin, inducing itch in-vivo, as a pruritogen [22]. Periostin release from keratinocytes and fibroblasts is further stimulated by TSLP and other canonical Th2-cytokines (IL-4, IL-13) in a paracrine fashion, in a vicious cycle feedback loop, as discussed in the next section [23].…”

Section: Th2 Immunity As a Driver Of Chronic Pruritusmentioning

confidence: 99%

Pruritus as a Distinctive Feature of Type 2 Inflammation

et al. 2021

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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.

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Section: Th2 Immunity As a Driver Of Chronic Pruritusmentioning

confidence: 99%

Pruritus as a Distinctive Feature of Type 2 Inflammation

et al. 2021

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“…Lumbar DRGs were isolated from naïve, control, and MIA-injected mice, sectioned on a cryostat at 12 μm thickness for double immunofluorescence labeling (46). Primary antibodies were diluted (1:500 each) in 5% blocking solution.…”

Section: Methodsmentioning

confidence: 99%

Artemin and its cognate receptor, GFRα3, play a function role in osteoarthritis pain

Minnema

Mishra

Lascelles

2020

Preprint

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Osteoarthritis associated pain (OA-pain) is a significant global problem. OA-pain limits limb use and mobility, and is associated with widespread sensitivity. Therapeutic options are limited, and the ones that are available are often associated with side or adverse effects. The lack of therapeutic options is partly due to a lack of understanding of clinically relevant underlying neural mechanisms of OA-pain. In previous work in naturally occurring OA-pain in dogs, we identified potential signaling molecules (artemin/GFRα3) that were upregulated. Here, we use multiple approaches including knockout mice, immunological suppression in a mouse model of OA, and clinically relevant measures of sensitivity and limb use to explore the functional role of artemin/GFRα3 signaling in OA-pain. We found the monoiodoacetate (MIA)-induced OA model in mice is associated with decreased limb use and hypersensitivity. GFRα3 expression is increased in sensory neurons. Exogenous artemin induces heat, cold and mechanical hypersensitivity, and anti-artemin monoclonal antibody administration reverses this hypersensitivity and restores limb use in mice with MIA-induced OA pain. Our results provide a molecular basis of arthritis pain linked with artemin/GFRα3 signaling and indicate that further work is warranted to investigate the neuronal plasticity and the pathways that drive pain in OA.

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“…Because periostin induces TSLP secretion by keratinocytes, an amplification loop involving periostin and TSLP is considered to be a mechanism of the dermal remodeling and epidermal hyperplasia typical of chronic AD 45,105,106 . Recently, it was demonstrated that periostin induced itch in mice, dogs and monkeys and the integrin aVb3 was identified as the periostin neuronal receptor 94 . In addition, given that keratinocytes release periostin in response to TSLP, it was found that an amplification loop involving periostin and TSLP may also be involved in chronic allergic itch 94 …”

Section: Intense Itch In Admentioning

confidence: 99%

“…45,105,106 Recently, it was demonstrated that periostin induced itch in mice, dogs and monkeys and the integrin aVb3 was identified as the periostin neuronal receptor. 94 In addition, given that keratinocytes release periostin in response to TSLP, it was found that an amplification loop involving periostin and TSLP may also be involved in chronic allergic itch. 94…”

Section: Periostinmentioning

confidence: 99%

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Basics and recent advances in the pathophysiology of atopic dermatitis

Nakahara

Kido‐Nakahara

Tsuji

et al. 2020

The Journal of Dermatology

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Atopic dermatitis is a common, chronic inflammatory skin disease that is characterized by skin barrier dysfunction, inflammation and intense itch. Although the exact mechanisms behind its pathogenesis remain unclear, it is evident that the complex interplay among barrier dysfunction, inflammation and itch are critical in its development, progression and chronicity. Abnormalities in filaggrin, intercellular lipids and tight junctions induce barrier‐disrupted skin, which produces thymic stromal lymphopoietin, interleukin (IL)‐25 and IL‐33; these in turn promote skin inflammation characterized by type 2 immune deviation. This inflammation then downregulates the expression of filaggrin in keratinocytes and exacerbates epidermal barrier dysfunction. Furthermore, various itch mediators/pruritogens produced during this inflammatory process can act directly on sensory nerves and cause itch. In this review, we summarize the basics and recent advances in our understanding of the pathophysiology of atopic dermatitis focusing on three aspects: barrier dysfunction, skin inflammation and itch.

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Periostin Activation of Integrin Receptors on Sensory Neurons Induces Allergic Itch

Cited by 80 publications

References 99 publications

Pruritus as a Distinctive Feature of Type 2 Inflammation

Pruritus as a Distinctive Feature of Type 2 Inflammation

Artemin and its cognate receptor, GFRα3, play a function role in osteoarthritis pain

Basics and recent advances in the pathophysiology of atopic dermatitis

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