Insights into atopic dermatitis gained from genetically defined mouse models

Nakajima, Saeko; Nomura, Takashi; Common, John E.A.; Kabashima, Kenji

doi:10.1016/j.jaci.2018.11.014

Cited by 61 publications

(61 citation statements)

References 165 publications

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“…Therefore, it is difficult for these mouse models to clearly reappear atopic dermatitis. Although the mouse models are not a complete imitation of the overall clinical symptoms, it does provide a basic core of phenotypic expression [37,38]. Thus, using the mouse models, we tested the effects of acorn shell extract (ASE) that induces AD-like skin lesions with oxazolone and DNCB.…”

Section: Effects Of Ase Application On Oxazolone-induced Ad-like Skinmentioning

confidence: 99%

Anti-Atopic Effect of Acorn Shell Extract on Atopic Dermatitis-Like Lesions in Mice and Its Active Phytochemicals

et al. 2019

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To investigate the potential effects of acorn shells on atopic dermatitis (AD), we utilized oxazolone (OX)-or 2,4-dinitrochlorobenzene (DNCB)-induced AD-like lesion mouse models. Our research demonstrates that Acorn shell extract (ASE) improved the progression of AD-like lesions, including swelling, which were induced by oxazolone on Balb/c mouse ears. Additionally, ASE significantly decreased the ear thickness (OX: 0.42 ± 0.01 mm, OX-ASE: 0.32 ± 0.02 mm) and epidermal thickness (OX: 75.3 ± 32.6 µm, OX-ASE: 46.1 ± 13.4 µm). The continuous DNCB-induced AD mouse model in SKH-1 hairless mice demonstrated that ASE improved AD-like symptoms, including the recovery of skin barrier dysfunction, Immunoglobulin E hyperproduction (DNCB: 340.1 ± 66.8 ng/mL, DNCB-ASE: 234.8 ± 32.9 ng/mL) and an increase in epidermal thickness (DNCB: 96.4 ± 21.9 µm, DNCB-ASE: 52.4 ± 16.3 µm). In addition, we found that ASE suppressed the levels of AD-involved cytokines, such as Tumor Necrosis Factor α, IL-1β, IL-25 and IL-33 in both animal models. Furthermore, gallic acid and ellagic acid isolated from ASE suppressed β-hexosaminidase release and IL-4 expression in RBL-2H3 cells. The acorn shell and its active phytochemicals have potential as a new remedy for the improvement of atopic dermatitis and other inflammatory diseases.

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Section: Effects Of Ase Application On Oxazolone-induced Ad-like Skinmentioning

confidence: 99%

Anti-Atopic Effect of Acorn Shell Extract on Atopic Dermatitis-Like Lesions in Mice and Its Active Phytochemicals

et al. 2019

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“…There is no evidence that any one of the pathological conditions of AD is upstream. AD is a multifactorial, complex inflammatory skin disease; its pathogenesis includes impaired skin barrier function, excess type 2 cytokine production, and pruritus/excoriation [3]. In this review, we summarize how IL-33 is involved in the complex pathogenesis of AD.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-33 in atopic dermatitis

Imai

2019

Journal of Dermatological Science

143

110

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Atopic dermatitis (AD) is characterized by pruritus, barrier disruption, and inflammationincluding type 2 cytokine production. Interleukin-33 (IL-33) is an inflammatory cytokine that is over-expressed in the keratinocytes of patients with AD. IL-33 transgenic mice, which express IL-33 specifically in keratinocytes, spontaneously develop AD-like eczema, suggesting that IL-33 is sufficient for the development of AD. IL-33 stimulates various cells, including group 2 innate lymphoid cells (ILC2s), to produce type 2 cytokines, such as IL-5 and IL-13, and IL-33-stimulated basophils activate ILC2s via IL-4. ILC2s are enriched in human AD skin lesions, and ILC2 isolated from AD lesions, are activated by IL-33, not by thymic stromal lymphopoietin (TSLP). IL-33 induces IL-31, thereby promoting pruritus and scratching behavior. Conversely, scratching the skin promotes IL-33 release from keratinocytes. IL-33 reduces the expression of filaggrin and claudin-1; it also reduces the skin barrier function. However, barrier destruction causes percutaneous exposure to allergens or IL-33 release. Thus, IL-33 is a common point of entry into the itch-scratch cycle of AD. These new findings can facilitate the development of novel therapeutic drugs targeting IL-33.

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“…Dear Editor, Atopic dermatitis (AD) is a chronic pruritic inflammatory skin disease characterized by barrier dysfunction, an allergic property that involves mainly Th2-type inflammatory response, and pruritus. 1 Dupilumab, a fully human IgG4 monoclonal antibody that inhibits both interleukin (IL)-4 and IL-13 signaling, has recently been used for the treatment of adult patients with moderateto-severe AD. 2 Dupilumab has been shown to progressively improve systemic and cutaneous abnormalities in patients with AD.…”

Section: Two Atopic Dermatitis Patients In Whom Dupilumab Improved Abmentioning

confidence: 99%

Two atopic dermatitis patients in whom dupilumab improved aberrant epidermal protease activities

Nomura

Kawakami

Yasutomi

et al. 2019

J Cutaneous Imm & Allergy

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Insights into atopic dermatitis gained from genetically defined mouse models

Cited by 61 publications

References 165 publications

Anti-Atopic Effect of Acorn Shell Extract on Atopic Dermatitis-Like Lesions in Mice and Its Active Phytochemicals

Anti-Atopic Effect of Acorn Shell Extract on Atopic Dermatitis-Like Lesions in Mice and Its Active Phytochemicals

Interleukin-33 in atopic dermatitis

Two atopic dermatitis patients in whom dupilumab improved aberrant epidermal protease activities

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