Evidence map›Paper›PMID 42909683›Full record

ArticleCell biology and toxicology2026

TRPC5 mediates MUC5AC secretion via NLRP3 inflammasome in toluene diisocyanate-induced mixed granulocytic asthma.

Shuyu Chen, Zhengqiang He, Kai Yang, Yuanyuan Liu, Li Yu, Linlin Zheng, Wei Ma, Zhou Cai, Shanze Chen, Lingwei Wang and 1 more

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Article in Cell biology and toxicology, 2026. 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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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Shuyu Chen *Department of Pulmonary and Critical Care Medicine, The Second Clinical Medical College, Shenzhen Institute of Respiratory Diseases, Shenzhen Peoples Hospital, Jinan University, The First Affiliated Hospital of SouthernUniversity of Science and Technology, Shenzhen, 518020, China. hxshuyuchen@126.com.
Zhengqiang He *Department of Pulmonary and Critical Care Medicine, The Second Clinical Medical College, Shenzhen Institute of Respiratory Diseases, Shenzhen Peoples Hospital, Jinan University, The First Affiliated Hospital of SouthernUniversity of Science and Technology, Shenzhen, 518020, China.
Kai Yang *Department of Pulmonary and Critical Care Medicine, The Second Clinical Medical College, Shenzhen Institute of Respiratory Diseases, Shenzhen Peoples Hospital, Jinan University, The First Affiliated Hospital of SouthernUniversity of Science and Technology, Shenzhen, 518020, China.
Yuanyuan Liu *Department of Pulmonary and Critical Care Medicine, The Second Clinical Medical College, Shenzhen Institute of Respiratory Diseases, Shenzhen Peoples Hospital, Jinan University, The First Affiliated Hospital of SouthernUniversity of Science and Technology, Shenzhen, 518020, China.
Li YuDepartment of Pulmonary and Critical Care Medicine, The Second Clinical Medical College, Shenzhen Institute of Respiratory Diseases, Shenzhen Peoples Hospital, Jinan University, The First Affiliated Hospital of SouthernUniversity of Science and Technology, Shenzhen, 518020, China.
Linlin ZhengDepartment of Pulmonary and Critical Care Medicine, The Second Clinical Medical College, Shenzhen Institute of Respiratory Diseases, Shenzhen Peoples Hospital, Jinan University, The First Affiliated Hospital of SouthernUniversity of Science and Technology, Shenzhen, 518020, China.
Wei MaTranslational Medicine Collaborative Innovation Center, The Second Clinical Medical College, Shenzhen Peoples Hospital, Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, 518020, China.
Zhou CaiDepartment of Pulmonary and Critical Care Medicine, Zhujiang Hospital, Southern Medical University, Haizhu District, 253 Gongye Middle Avenue, Guangzhou, 510280, China.
Shanze ChenDepartment of Pulmonary and Critical Care Medicine, The Second Clinical Medical College, Shenzhen Institute of Respiratory Diseases, Shenzhen Peoples Hospital, Jinan University, The First Affiliated Hospital of SouthernUniversity of Science and Technology, Shenzhen, 518020, China.
Lingwei WangDepartment of Pulmonary and Critical Care Medicine, The Second Clinical Medical College, Shenzhen Institute of Respiratory Diseases, Shenzhen Peoples Hospital, Jinan University, The First Affiliated Hospital of SouthernUniversity of Science and Technology, Shenzhen, 518020, China. wang.lingwei@szhospital.com.
Rongchang ChenDepartment of Pulmonary and Critical Care Medicine, The Second Clinical Medical College, Shenzhen Institute of Respiratory Diseases, Shenzhen Peoples Hospital, Jinan University, The First Affiliated Hospital of SouthernUniversity of Science and Technology, Shenzhen, 518020, China. chenrc@vip.163.com.

Funding

National Natural Science Foundation of China 82100023Shenzhen Medical Research Funds A2303030Shenzhen Science and Technology Program JCYJ20250604142040011
6 · The paper itself

Abstract

BACKGROUND AND

objectiveAirway mucus overproduction (predominantly MUC5AC) is a well-recognized pathogenic feature in asthma, but the upstream regulatory mechanisms were enigmatic. Emerging evidence has implied the crucial role for transient receptor potential canonical channel 5 (TRPC5) in the pathogenesis of allergic diseases. Yet, the specific role of TRPC5 in asthma still remains unclear. Thus, this study was aimed to explore the functional role of TRPC5 in toluene diisocyanate (TDI)-induced mixed granulocytic asthma and to delineate the mechanisms by which TRPC5 regulate MUC5AC secretion.

methodsBronchoalveolar lavage fluid (BALF) and mucosal biopsy samples were collected from asthmatic subjects and control. Using a murine model of TDI-induced asthma, we gave the asthmatic mice selective TRPC5 inhibitors ML204, AC1903 or an NLRP3 inhibitor, MCC950. In vitro experiments were performed in a human airway epithelial cell line BEAS-2B.

resultsBALF levels of MUC5AC were significantly increased in the recruited asthmatic patients, as well as the levels of HMGB1, and a positive correlation was observed between the two. Expression of TRPC5 was elevated in the airway epithelium of asthmatics when compared to the control. In mice, TDI exposure raised the expression of TRPC5. Blocking TRPC5 with either ML204 or AC1903 dramatically attenuated TDI-induced airway hyperresponsiveness (AHR), airway inflammation and remodeling. Additionally, both antagonists led to inhibited activation of NLRP3 inflammasome and muc5ac secretion in TDI-exposed mice. While pharmacological inhibition of NLRP3 inflammasome suppressed TDI-induced muc5ac secretion. In vitro, TDI induced increased expression of MUC5AC, NLRP3 and TRPC5 in BEAS-2B. Silence of either trpc5 or nlrp3 effectively inhibited MUC5AC hypersecretion in airway epithelium induced by TDI. Besides, TRPC5 agonist (Riluzole) promoted MUC5AC overproduction in airway epithelial cells, which could be suppressed by nlrp3 siRNA.

conclusionTRPC5 contributes to TDI-induced asthma, and mediates airway epithelial muc5ac hypersecretion by partially activating NLRP3 inflammasome.

Indexed as

AsthmaGranulocytesInflammasomesMucin 5ACNLR Family, Pyrin Domain-Containing 3 ProteinTRPC Cation ChannelsAdultAnimalsBronchoalveolar Lavage FluidCell LineDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred BALB CInflammasomesMUC5AC protein, humanMucin 5ACNLR Family, Pyrin Domain-Containing 3 ProteinToluene 2,4-DiisocyanateTRPC Cation ChannelsAsthmaMUC5AC secretionToluene diisocyanateTRPC5

Identifiers

PMID42909683

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