Thymic stromal lymphopoietin-activated basophil promotes lung inflammation in mouse atopic march model

BackgroundAtopic dermatitis (AD), a prevalent inflammatory skin disease affecting 10%-20% of the population, is linked to the development of asthma through atopic march (AM). This study aims to explore the role of basophils in OVA-induced lung inflammation in the presence of AD-like skin lesions and...

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Main Authors: Xu Li, Zizhuo Li, Mindan Tang, Kaoyuan Zhang, Ting Yang, Weilong Zhong, Bo Yu, Fang Wang, Xia Dou
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-05-01
Series:Frontiers in Immunology
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Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2025.1573130/full
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author Xu Li
Zizhuo Li
Mindan Tang
Kaoyuan Zhang
Kaoyuan Zhang
Kaoyuan Zhang
Ting Yang
Weilong Zhong
Bo Yu
Bo Yu
Bo Yu
Fang Wang
Xia Dou
Xia Dou
Xia Dou
author_facet Xu Li
Zizhuo Li
Mindan Tang
Kaoyuan Zhang
Kaoyuan Zhang
Kaoyuan Zhang
Ting Yang
Weilong Zhong
Bo Yu
Bo Yu
Bo Yu
Fang Wang
Xia Dou
Xia Dou
Xia Dou
author_sort Xu Li
collection DOAJ
description BackgroundAtopic dermatitis (AD), a prevalent inflammatory skin disease affecting 10%-20% of the population, is linked to the development of asthma through atopic march (AM). This study aims to explore the role of basophils in OVA-induced lung inflammation in the presence of AD-like skin lesions and investigate the potential contribution of thymic stromal lymphopoietin (TSLP) in activating basophils.MethodsMouse AM models were established in C57BL/6 mice using MC903 and OVA epicutaneous sensitization, followed by intranasal OVA challenges. An intraperitoneal OVA-sensitized asthma model was employed as the control group. RNA-Seq analysis was conducted on lung CD45+ immune cells from these models. Histologic examinations, flow cytometry, and ELISA were used to examine the lung and systemic inflammatory response. Basophil depletion was achieved through intraperitoneal administration of anti-FcϵRIα mAb. The role of TSLP was investigated using TSLPR knockout mice.ResultsAs in the intraperitoneal sensitization model, AM model also induced eosinophilic lung inflammation in mice, resembling the AM process. The RNA-Seq analysis revealed differential gene expression, with genes related to basophils being prominent in AM model. Increased basophil activation and IL-4 production were observed in OVA epicutaneously sensitized mice. Basophil depletion attenuated the eosinophilic lung inflammation. TSLP levels increased with topical MC903, and TSLPR knockout reduced lung inflammation, suggesting TSLP is involved in basophil activation.ConclusionBasophils play a crucial role in OVA-induced lung inflammation in the context of AD-like skin lesions, and TSLP appears to drive basophil activation. Understanding these interactions provides insights for potential therapeutic interventions in AM-associated conditions.
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spelling doaj-art-14e728862dfa44a5a32cd6f85f3cac962025-08-20T03:49:42ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-05-011610.3389/fimmu.2025.15731301573130Thymic stromal lymphopoietin-activated basophil promotes lung inflammation in mouse atopic march modelXu Li0Zizhuo Li1Mindan Tang2Kaoyuan Zhang3Kaoyuan Zhang4Kaoyuan Zhang5Ting Yang6Weilong Zhong7Bo Yu8Bo Yu9Bo Yu10Fang Wang11Xia Dou12Xia Dou13Xia Dou14Department of Dermatology, Peking University Shenzhen Hospital, Shenzhen, ChinaDepartment of Dermatology, Peking University Shenzhen Hospital, Shenzhen, ChinaDepartment of Dermatology, Peking University Shenzhen Hospital, Shenzhen, ChinaDepartment of Dermatology, Peking University Shenzhen Hospital, Shenzhen, ChinaInstitute of Dermatology, Shenzhen Peking University-the Hong Kong University of Science and Technology Medical Center, Shenzhen, ChinaShenzhen Key Laboratory for Translational Medicine of Dermatology, Biomedical Research Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology Medical Center, Shenzhen, ChinaDepartment of Dermatology, Peking University Shenzhen Hospital, Shenzhen, ChinaDepartment of Dermatology, Peking University Shenzhen Hospital, Shenzhen, ChinaDepartment of Dermatology, Peking University Shenzhen Hospital, Shenzhen, ChinaInstitute of Dermatology, Shenzhen Peking University-the Hong Kong University of Science and Technology Medical Center, Shenzhen, ChinaShenzhen Key Laboratory for Translational Medicine of Dermatology, Biomedical Research Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology Medical Center, Shenzhen, ChinaDepartment of Dermatology, Dermatology Hospital of Southern Medical University, Guangzhou, ChinaDepartment of Dermatology, Peking University Shenzhen Hospital, Shenzhen, ChinaInstitute of Dermatology, Shenzhen Peking University-the Hong Kong University of Science and Technology Medical Center, Shenzhen, ChinaShenzhen Key Laboratory for Translational Medicine of Dermatology, Biomedical Research Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology Medical Center, Shenzhen, ChinaBackgroundAtopic dermatitis (AD), a prevalent inflammatory skin disease affecting 10%-20% of the population, is linked to the development of asthma through atopic march (AM). This study aims to explore the role of basophils in OVA-induced lung inflammation in the presence of AD-like skin lesions and investigate the potential contribution of thymic stromal lymphopoietin (TSLP) in activating basophils.MethodsMouse AM models were established in C57BL/6 mice using MC903 and OVA epicutaneous sensitization, followed by intranasal OVA challenges. An intraperitoneal OVA-sensitized asthma model was employed as the control group. RNA-Seq analysis was conducted on lung CD45+ immune cells from these models. Histologic examinations, flow cytometry, and ELISA were used to examine the lung and systemic inflammatory response. Basophil depletion was achieved through intraperitoneal administration of anti-FcϵRIα mAb. The role of TSLP was investigated using TSLPR knockout mice.ResultsAs in the intraperitoneal sensitization model, AM model also induced eosinophilic lung inflammation in mice, resembling the AM process. The RNA-Seq analysis revealed differential gene expression, with genes related to basophils being prominent in AM model. Increased basophil activation and IL-4 production were observed in OVA epicutaneously sensitized mice. Basophil depletion attenuated the eosinophilic lung inflammation. TSLP levels increased with topical MC903, and TSLPR knockout reduced lung inflammation, suggesting TSLP is involved in basophil activation.ConclusionBasophils play a crucial role in OVA-induced lung inflammation in the context of AD-like skin lesions, and TSLP appears to drive basophil activation. Understanding these interactions provides insights for potential therapeutic interventions in AM-associated conditions.https://www.frontiersin.org/articles/10.3389/fimmu.2025.1573130/fullatopic dermatitisatopic marchbasophileosinophilic lung inflammationthymic stromal lymphopoietin
spellingShingle Xu Li
Zizhuo Li
Mindan Tang
Kaoyuan Zhang
Kaoyuan Zhang
Kaoyuan Zhang
Ting Yang
Weilong Zhong
Bo Yu
Bo Yu
Bo Yu
Fang Wang
Xia Dou
Xia Dou
Xia Dou
Thymic stromal lymphopoietin-activated basophil promotes lung inflammation in mouse atopic march model
Frontiers in Immunology
atopic dermatitis
atopic march
basophil
eosinophilic lung inflammation
thymic stromal lymphopoietin
title Thymic stromal lymphopoietin-activated basophil promotes lung inflammation in mouse atopic march model
title_full Thymic stromal lymphopoietin-activated basophil promotes lung inflammation in mouse atopic march model
title_fullStr Thymic stromal lymphopoietin-activated basophil promotes lung inflammation in mouse atopic march model
title_full_unstemmed Thymic stromal lymphopoietin-activated basophil promotes lung inflammation in mouse atopic march model
title_short Thymic stromal lymphopoietin-activated basophil promotes lung inflammation in mouse atopic march model
title_sort thymic stromal lymphopoietin activated basophil promotes lung inflammation in mouse atopic march model
topic atopic dermatitis
atopic march
basophil
eosinophilic lung inflammation
thymic stromal lymphopoietin
url https://www.frontiersin.org/articles/10.3389/fimmu.2025.1573130/full
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