ArticleFrontiers in immunology2021
Epithelial Aryl Hydrocarbon Receptor Protects From Mucus Production by Inhibiting ROS-Triggered NLRP3 Inflammasome in Asthma.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Pseudomonas aeruginosa-derived volatile organic compounds modulate AhR signaling to dysregulate airway mucus homeostasis.Nature communications · 2026Article
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
- The Mechanism of NLRP3 Inflammasome Activation and Its Roles in Chronic Rhinosinusitis.World journal of otorhinolaryngology - head and neck surgery · 2026Review
- PPAR-γ suppresses macrophage senescence and allergic airway inflammation through controlling lipid metabolic pathways.EBioMedicine · 2026Article
- ROMO1 is involved in airway mucus hypersecretion in COPD through the mitochondrial ROS-STAT6 pathway.Respiratory research · 2026Article
- The Role of Aryl Hydrocarbon Receptor in Airway Remodeling: Mechanistic Insights Across Cellular Functions.Clinical reviews in allergy & immunology · 2026Review
- NLRP3-mediated epithelial pyroptosis involved in airway hyperresponsiveness in combined eosinophilic and neutrophilic asthma.Cell communication and signaling : CCS · 2026Article
- Oxidative stress driven airway mesenchymal reprogramming in asthma: mechanistic insights and evidence from botanical drug formulations.Frontiers in pharmacology · 2026Review
- Epithelial AhR Suppresses Allergen-Induced Oxidative Stress and Senescence via c-Myc Regulation.Antioxidants (Basel, Switzerland) · 2025Article
- Susceptibility to childhood asthma modified by the interactive effects of polycyclic aromatic hydrocarbons exposure and genetic polymorphisms of the aryl hydrocarbon receptor signaling pathway: functional analysis based on lipid metabolism.Respiratory research · 2025Article
- Asthma and inflammation transcriptionally up-regulate the aryl hydrocarbon receptor in airway smooth muscle via p38/JNK-AP1 signalling.British journal of pharmacology · 2025Article
- The Ubiquitin-Proteasome System in Asthma: Mechanisms and Therapeutic Possibilities.Clinical reviews in allergy & immunology · 2025Review
- Safranal restores RUNX3-mediated immunoregulation by inhibiting the NLRP3 inflammasome in allergic asthma.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Mulberroside A ameliorates murine allergic airway inflammation by suppressing Th2 response and oxidative stress.Inflammopharmacology · 2025Article
- Mucins and Their Roles in Asthma.Immunological reviews · 2025Review
- Multifaceted roles of mitochondria in asthma.Cell biology and toxicology · 2024Review
- NOX2 mediates NLRP3/ROS facilitating nasal mucosal epithelial inflammation in chronic rhinosinusitis with nasal polyps.Heliyon · 2024Article
- The NLRP3 inflammasome in allergic diseases: mechanisms and therapeutic implications.Clinical and experimental medicine · 2024Review
- Aryl Hydrocarbon Receptor Activation in Pulmonary Alveolar Epithelial Cells Limits Inflammation and Preserves Lung Epithelial Cell Integrity.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Impaired tryptophan metabolism by type 2 inflammation in epithelium worsening asthma.iScience · 2024Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Background: Despite long-standing recognition in the significance of mucus overproduction in asthma, its etiology remains poorly understood. Muc5ac is a secretory mucin that has been associated with reduced pulmonary function and asthma exacerbations. Objectives: We sought to investigate the immunological pathway that controls Muc5ac expression and allergic airway inflammation in asthma. Methods: Cockroach allergen-induced Muc5ac expression and aryl hydrocarbon receptor (AhR) signaling activation was examined in the human bronchial epithelial cells (HBECs) and mouse model of asthma. AhR regulation of Muc5ac expression, mitochondrial ROS (Mito-ROS) generation, and NLRP3 inflammasome was determined by AhR knockdown, the antagonist CH223191, and AhR Results: Cockroach allergen induced Muc5ac overexpression in HBECs and airways of asthma mouse model. Increased expression of AhR and its downstream genes CYP1A1 and CYP1B1 was also observed. Mice with AhR deletion showed increased allergic airway inflammation and MUC5AC expression. Moreover, cockroach allergen induced epithelial NLRP3 inflammasome activation (e.g., NLRP3, Caspase-1, and IL-1β), which was enhanced by AhR knockdown or the antagonist CH223191. Furthermore, AhR deletion in HBECs led to enhanced ROS generation, particularly Mito-ROS, and inhibition of ROS or Mito-ROS subsequently suppressed the inflammasome activation. Importantly, inhibition of the inflammasome with MCC950, a NLRP3-specifc inhibitor, attenuated allergic airway inflammation and Muc5ac expression. IL-1β generated by the activated inflammasomes mediated cockroach allergen-induced Muc5ac expression in HBECs. Conclusions: These results reveal a previously unidentified functional axis of AhR-ROS-NLRP3 inflammasome in regulating Muc5ac expression and airway inflammation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.