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REVIEW article

Front. Immunol.
Sec. Inflammation
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1473105
This article is part of the Research Topic Innate immune dysregulation: a driving force of autoimmunity and chronic inflammation View all 7 articles

Molecular Mechanisms of Obesity Predisposes to Atopic Dermatitis

Provisionally accepted
Dajin Shang Dajin Shang 1Shengnan Zhao Shengnan Zhao 2*
  • 1 China Medical University, Shenyang, Liaoning Province, China
  • 2 The First Affiliated Hospital of China Medical University, Shenyang, China

The final, formatted version of the article will be published soon.

    Obesity is a prevalent metabolic disease that reduces bacterial diversity, colonizes the epidermis with lipophilic bacteria, and increases intestinal pro-inflammatory species, all of which lead to impaired epithelial barriers. Adipose tissue secretes immunomodulatory molecules, such as adipokines, leptin, and adiponectin, which alters the morphology of adipocytes and macrophages as well as modulates T cell differentiation and peripheral Th2-dominated immune responses.Atopic dermatitis (AD) and obesity have similar pathological manifestations, including inflammation as well as insulin and leptin resistance. This review examines the major mechanisms between obesity and AD, which focus on the effect on skin and gut microbiota, immune responses mediated by the toll like receptor (TLR) signaling pathway, and changes in cytokine levels (TNF-a, IL-6, IL-4, and IL13). Moreover, we describe the potential effects of adipokines on AD and finally mechanisms by which PPAR-γ suppresses and regulates type 2 immunity.

    Keywords: atopic dermatitis, Obesity, immune, Adipokines, Cytokines

    Received: 30 Jul 2024; Accepted: 15 Oct 2024.

    Copyright: © 2024 Shang and Zhao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Shengnan Zhao, The First Affiliated Hospital of China Medical University, Shenyang, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.