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ATAC-Seq Library Preparation of Murine Bone Marrow-Derived Neutrophils
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Neutrophils in Atopic Dermatitis.

Chih-Chao Chiang1,2, Wei-Jen Cheng3,4, Joseph Renz Marion Santiago Dela Cruz5

  • 1Department of Nutrition and Health Sciences, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan.

Clinical Reviews in Allergy & Immunology
|September 18, 2024
PubMed
Summary

Neutrophils play a key role in atopic dermatitis (AD) by releasing proteins that worsen itching and skin barrier defects. Targeting these neutrophils could be a new strategy for treating AD symptoms.

Keywords:
Neutrophil; Atopic dermatitis; Inflammation; PruritusSkin lesions

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Area of Science:

  • Immunology
  • Dermatology
  • Inflammation Research

Background:

  • Neutrophils are increasingly recognized for their role in inflammatory skin conditions.
  • Their specific function in atopic dermatitis (AD) pathophysiology requires further elucidation.
  • Distinct neutrophil presence in AD suggests a significant contribution to the disease.

Purpose of the Study:

  • To review and synthesize current research on the role of neutrophils in AD.
  • To elucidate the mechanisms by which neutrophils contribute to AD symptoms and progression.
  • To identify neutrophils as potential therapeutic targets for AD management.

Main Methods:

  • Literature review of studies investigating neutrophil involvement in AD.
  • Analysis of protein expression (myeloperoxidase, elastase, lipocalin, HMGB1) in AD skin.
  • Examination of neutrophil-mast cell interactions and immune pathway activation (Th2, Th17).

Main Results:

  • Neutrophil-derived proteins (e.g., myeloperoxidase, elastase) exacerbate pruritus in AD.
  • Neutrophilic oxidative stress and neutrophil extracellular traps (NETs) worsen AD.
  • Elevated neutrophil elastase and HMGB1 in AD skin impair epidermal barrier function.
  • Neutrophil-mast cell interactions promote Th2/Th17 imbalance, particularly with allergens/infections.
  • Therapies that reduce pruritus in AD also inhibit neutrophil activity.

Conclusions:

  • Neutrophils are significant contributors to AD pathogenesis, driving inflammation and pruritus.
  • Neutrophil-derived molecules and processes directly impact skin barrier integrity.
  • Neutrophils represent a promising therapeutic target for alleviating AD symptoms and improving treatment strategies.