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ORIGINAL RESEARCH article

Front. Immunol.
Sec. Inflammation
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1439367

Role of LECT2 in Exacerbating Atopic Dermatitis: Insight from In Vivo and In Vitro Models via NF-κB Signaling Pathway

Provisionally accepted
Zhifang Liu Zhifang Liu 1Jiang Xinyu Jiang Xinyu 1Keyu Zhao Keyu Zhao 1Hongyu Ruan Hongyu Ruan 1Yizhao Ma Yizhao Ma 1Yuhan Ma Yuhan Ma 1Qiongyan Zhou Qiongyan Zhou 1Jing Zhang Jing Zhang 1Xiaoyan Sun Xiaoyan Sun 1Wenxue Ma Wenxue Ma 2*Suling Xu Suling Xu 1
  • 1 The First Affiliated Hospital of Ningbo University, Ningbo, China
  • 2 University of California, San Diego, La Jolla, United States

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

    Leukocyte cell-derived chemotaxin 2 (LECT2) is linked to various immune diseases. Previously, we reported that serum LECT2 levels correlate with disease severity in atopic dermatitis (AD) patients. To investigate the role of LECT2 in AD and elucidate its potential mechanisms, we used LECT2 to treat an AD mouse model induced by 1-Chloro-2,4-dinitrobenzene (DNCB) in LECT2 knockout (KO) and wild-type (WT) mice, and an AD cell model using TNF-α/IFN-γ-induced HaCaT cells. Inflammatory factors and barrier proteins were analyzed by histology, immunohistochemistry, RT-qPCR, ELISA, and Western Blot. Activation of the NF-κB signaling pathway was evaluated by Western Blot and immunofluorescence. In the AD mouse model, LECT2 treatment increased epidermal and dermal thickness, mast cell infiltration, and downregulated barrier proteins. Inflammatory factors were increased in skin lesions and serum. In the AD cell model, LECT2 decreased barrier protein levels and increased inflammatory factor levels, enhancing NF-κB P65 nuclear translocation. These results indicate that LECT2 exacerbates AD-like responses by dysregulating the NF-κB signaling pathway, highlighting its potential as a therapeutic target for AD management.

    Keywords: atopic dermatitis, NF-κB signaling pathway, inflammatory cytokines, skin barrier proteins, Therapeutic target

    Received: 27 May 2024; Accepted: 29 Jul 2024.

    Copyright: © 2024 Liu, Xinyu, Zhao, Ruan, Ma, Ma, Zhou, Zhang, Sun, Ma and Xu. 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: Wenxue Ma, University of California, San Diego, La Jolla, United States

    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.