Atopic Dermatitis Model

Introduction

Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder characterized by persistent pruritus. It typically occurs in children and adolescents but may also manifest in adults. The pathogenesis of atopic dermatitis is complex and may involve multiple factors, including genetics, environment, and immune dysregulation.

Disease models

The SMOC has long been dedicated to autoimmune disease research and has developed a variety of mouse models of atopic dermatitis using agents such as oxazolone (OXA) and 2,4-dinitrofluorobenzene (DNFB), providing powerful tools for the efficacy evaluation and safety assessment of related drugs.

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Fig.1 OXA induced AD model in hIL4/hIL4R mice. (A) body weight (B) body weight change.

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Fig.2 OXA induced AD model in hIL4/hIL4R mice. (A) gross observation on Day 21  (B) ear thickness (C) clinical score of skin.

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Fig.3 OXA induced AD model in hIL4/hIL4R mice. (A) serum IgE (B) spleen weight.

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Fig.4 OXA induced AD model in hIL4/hIL4R mice. (A) Pathology photos (B) Pathology score.

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Fig.1 Body weight of hIL4/hIL4Ra mice treated with dupilumab. *P<0.05.

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Fig.2 Dupilumab ameliorate overall atopic dermatitis activity in DNFB-induced AD Model. *P<0.05, **P<0.01, ***P<0.001.

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Fig.3 Dupilumab treatment significantly reduced IgE levels in serum and scratching times. (A) day10 serum IgE (B) day16 serum IgE (C) scratch times on Day 12 (D) scratch times on Day 14. *P<0.05, **P<0.01, ***P<0.001.

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Fig.4 Dupilumab significantly mitigates inflammatory cell infiltration in lesioned skin on day 14. (A) dorsal image on day14; (B) Representative pathology images; (C) Inflammatory cell infiltration score; (D) neutrophils score; (E) eosinophils score; (F) epidermis thickness; (G) dermis thickness. *P<0.05, **P<0.01, ***P<0.001.

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Fig.1 DNFB induced AD model in BALB/c mice. (A) body weight (B) ear thickness (C) clinical score of skin (D) photographs of the mouse’s back and H&E-stained histological sections of the ear skin (E) serum IgE (E–H)statistical analysis of the degree of immune cell infiltration and dermal thickness.

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Fig.1 OXA induced AD model in C57BL/6 mice. (A–B) Changes in ear thickness and clinical scores in mice. (C) Photographs of the mice’s backs. (D–E) Measurement of serum IgE levels and spleen weight in mice. (F–H) H&E-stained histological sections of mouse skin and statistical analysis of the degree of immune cell infiltration and dermal thickness. The results indicate that dexamethasone significantly alleviated the skin lesions associated with OXA-induced specific dermatitis.


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Fig1. The efficacy of Crisaborole on MC903-induced AD model in C57BL/6 wild-type mice. (A) body weight (B) body weight change 

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Fig2. The efficacy of Crisaborole on MC903-induced AD model in C57BL/6 wild-type mice. (A) ear thickness (B) ear thickness change

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Fig3. The efficacy of Crisaborole on MC903-induced AD model in C57BL/6 wild-type mice. (A) erythema score (B) skin thickness score (C) scabby score (D) clinical score

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Fig4. The efficacy of Crisaborole on MC903-induced AD model in C57BL/6 wild-type mice. (A) serum mIgE (B) spleen index

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Fig5. The efficacy of Crisaborole on MC903-induced AD model in C57BL/6 wild-type mice. (A) ear mTGF-β (B) ear mIL13 (C) ear mIL5 (D) ear mIL25 (E) ear mIL2 (F) ear mIL33 (G) ear mTSLP (H) ear mTNFa (I) ear mIL8

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Fig6. The efficacy of Crisaborole on MC903-induced AD model in C57BL/6 wild-type mice. (A) inflammatory cell infiltration score (B) neutrophils score (C) eosinophils score (D) dermis thickness (E) epidermis thickness (F) typical pathology image

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