ArticleAllergy, asthma & immunology research2025
Interleukin-17D Attenuates OVA-induced Airway Inflammation and Remodeling Partially via the CD93 Receptor.
Shuochuan Shi, Jintao Zhang, Yun Pan, Xiaofei Liu, Rong Zeng, Changjuan Xu, Ying Wang, Qian Qi, Zhi Guo, Chengfang Yao and 4 more
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In one paragraphArticle in Allergy, asthma & immunology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 · Who and what moneyAuthors and funding
14 authors.
Shuochuan ShiDepartment of Respiratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Respiratory Diseases, Featured Laboratory of Respiratory Immunology and Regenerative Medicine in Universities of Shandong, Jinan Clinical Research Center for Respiratory Disease, Jinan, China.ORCID https://orcid.org/0009-0000-4648-4125 Jintao ZhangDepartment of Respiratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Respiratory Diseases, Featured Laboratory of Respiratory Immunology and Regenerative Medicine in Universities of Shandong, Jinan Clinical Research Center for Respiratory Disease, Jinan, China.ORCID https://orcid.org/0000-0002-1309-6836 Yun PanDepartment of Respiratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Respiratory Diseases, Featured Laboratory of Respiratory Immunology and Regenerative Medicine in Universities of Shandong, Jinan Clinical Research Center for Respiratory Disease, Jinan, China.ORCID https://orcid.org/0000-0002-5014-0322 Xiaofei LiuDepartment of Respiratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Respiratory Diseases, Featured Laboratory of Respiratory Immunology and Regenerative Medicine in Universities of Shandong, Jinan Clinical Research Center for Respiratory Disease, Jinan, China.ORCID https://orcid.org/0000-0002-7285-7578 Changjuan XuDepartment of Respiratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Respiratory Diseases, Featured Laboratory of Respiratory Immunology and Regenerative Medicine in Universities of Shandong, Jinan Clinical Research Center for Respiratory Disease, Jinan, China.ORCID https://orcid.org/0000-0001-8414-2986 Ying WangDepartment of Respiratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Respiratory Diseases, Featured Laboratory of Respiratory Immunology and Regenerative Medicine in Universities of Shandong, Jinan Clinical Research Center for Respiratory Disease, Jinan, China.ORCID https://orcid.org/0009-0006-6200-4279 Qian QiDepartment of Respiratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Respiratory Diseases, Featured Laboratory of Respiratory Immunology and Regenerative Medicine in Universities of Shandong, Jinan Clinical Research Center for Respiratory Disease, Jinan, China.ORCID https://orcid.org/0000-0002-5813-3194 Zhi GuoDepartment of Respiratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Respiratory Diseases, Featured Laboratory of Respiratory Immunology and Regenerative Medicine in Universities of Shandong, Jinan Clinical Research Center for Respiratory Disease, Jinan, China.ORCID https://orcid.org/0009-0008-2146-5962 Ju LiuInstitute of Microvascular Medicine, Medical Research Center, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, China.ORCID https://orcid.org/0000-0001-9932-2613 Li LiDepartment of Respiratory Medicine, Haihe Hospital, Tianjin Medical University, Key Research Laboratory for infectious Disease Prevention for State Administration of Traditional Chinese Medicine, Tianjin Institution of Respiratory Diseases, Tianjin Key Laboratory of Lung Regenerative Medicine, Tianjin, China. lili0718@tju.edu.cn.ORCID https://orcid.org/0009-0001-5767-9662 Liang DongDepartment of Respiratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Respiratory Diseases, Featured Laboratory of Respiratory Immunology and Regenerative Medicine in Universities of Shandong, Jinan Clinical Research Center for Respiratory Disease, Jinan, China. dl5506@126.com.ORCID https://orcid.org/0000-0001-7707-9982 Funding
China International Medical Foundation Z-2014-08-2309-1China International Medical Foundation Z-2017-24-2301Jinan Clinical Medicine Research Program for Respiratory Disease 202132002Key Research and Development Program of Shandong Province 2021SFGC0504National Natural Science Foundation of China 82270032National Natural Science Foundation of China 82470028Natural Science Foundation of Shandong Province ZR2024MH153Noncommunicable Chronic Diseases-National Science and Technology Major Project 2024ZD0529700Noncommunicable Chronic Diseases-National Science and Technology Major Project 2024ZD0529704Shandong Provincial Natural Science Foundation ZR2021LSW015
6 · The paper itselfAbstract
purposeAirway inflammation and remodeling are pivotal in asthma pathogenesis. Interleukin-17D (IL-17D), a recently characterized cytokine within the IL-17 family, is found to be expressed at higher levels in lung tissue; however, its role in asthma remains unclear. This study aims to elucidate the function and mechanisms of IL-17D in asthma, providing new insights for therapeutic strategies.
methodsWe analyzed IL-17D messenger RNA expression levels using datasets from the Gene Expression Omnibus (GEO). Bronchoscopic biopsy tissues and serum samples from asthmatics, along with lung tissues from chronic asthmatic mice, were collected to validate IL-17D expression. Lentivirus-mediated IL-17D knockdown was performed in a chronic asthma mouse model induced by ovalbumin (OVA). Recombinant murine IL-17D protein was intranasally administered to further investigate its impact.
resultsGEO data and experimental findings revealed that IL-17D expression was reduced in the airway epithelia of asthmatics and chronic asthmatic mice.
conclusionsOur findings suggest that IL-17D could play a protective role in asthmatic airway inflammation and remodeling, partially through the CD93 receptors. These results highlight IL-17D as a potential therapeutic target for asthma management.
Indexed as
airway remodelingAsthmaepithelial-mesenchymal transitionIL-17Dinflammation
Identifiers
PMID41044834
PMCPMC12511793
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