ArticleAmerican journal of respiratory cell and molecular biology2006
Persistent effects induced by IL-13 in the lung.
Article in American journal of respiratory cell and molecular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 104 citations in OpenAlex.
- A phase 1, randomized, placebo-controlled, dose-escalation study of an anti-IL-13 monoclonal antibody in healthy subjects and mild asthmatics.British journal of clinical pharmacology · 2013Trial
- Epigenetic and transcriptional programming of murine eosinophils in the esophagus.Nature communications · 2025Article
- Mouse models of eosinophilic esophagitis: molecular and translational insights.American journal of physiology. Gastrointestinal and liver physiology · 2025Review
- Outcome of SARS-CoV-2 reinfection depends on genetic background in female mice.Nature communications · 2024Article
- Host immune responses associated with SARS-CoV-2 Omicron infection result in protection or pathology during reinfection depending on mouse genetic background.Research square · 2023Article
- Review
- Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023Article
- Emerging Effects of IL-33 on COVID-19.International journal of molecular sciences · 2022Review
- The kinase p38α functions in dendritic cells to regulate Th2-cell differentiation and allergic inflammation.Cellular & molecular immunology · 2022Article
- Protective effects of glaucocalyxin A on the airway of asthmatic mice.Open medicine (Warsaw, Poland) · 2022Article
- Time-Dependent Increase in Susceptibility and Severity of Secondary Bacterial Infections During SARS-CoV-2.Frontiers in immunology · 2022Article
- Aiolos regulates eosinophil migration into tissues.Mucosal immunology · 2021Article
- Interleukin-13 as a target to alleviate severe coronavirus disease 2019 and restore lung homeostasis.Journal of clinical and translational research · 2021Article
- Prenatal and Postnatal Cigarette Smoke Exposure Is Associated With Increased Risk of Exacerbated Allergic Airway Immune Responses: A Preclinical Mouse Model.Frontiers in immunology · 2021Article
- Ex-vivo delivery of monoclonal antibody (Rituximab) to treat human donor lungs prior to transplantation.EBioMedicine · 2020Article
- Involvement of the epidermal growth factor receptor in IL-13-mediated corticosteroid-resistant airway inflammation.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2020Article
- Recombinant Pyrin Domain Protein Attenuates Airway Inflammation and Alleviates Epithelial-Mesenchymal Transition by Inhibiting Crosstalk Between TGFβ1 and Notch1 Signaling in Chronic Asthmatic Mice.Frontiers in physiology · 2020Article
- Interleukin-13 Alters Tight Junction Proteins Expression Thereby Compromising Barrier Function and Dampens Rhinovirus Induced Immune Responses in Nasal Epithelium.Frontiers in cell and developmental biology · 2020Article
- Interleukin-17: Friend or foe in organ fibrosis.Cytokine · 2019Review
- IL-13 Impairs Tight Junctions in Airway Epithelia.International journal of molecular sciences · 2019Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
IL-13 overexpression in the lung induces inflammatory and remodeling responses that are prominent features of asthma. Whereas most studies have concentrated on the development of IL-13-induced disease, far fewer studies have focused on the reversibility of IL-13-induced pathologies. This is particularly important because current asthma therapy appears to be poor at reversing lung remodeling. In this manuscript, we used an externally regulatable transgenic system that targets expression of IL-13 to the lung with the aim of characterizing the reversibility process. After 4 wk of doxycycline (dox) exposure, IL-13 expression resulted in mixed inflammatory cell infiltration, mucus cell metaplasia, lung fibrosis, and airspace enlargement (emphysema). After withdrawal of dox, IL-13 protein levels were profoundly reduced by 7 d and below baseline by 14 d. During this time frame, the level of lung eosinophils returned to near normal, whereas macrophages, lymphocytes, and neutrophils remained markedly elevated. IL-13-induced mucus cell metaplasia significantly decreased (91%) 3 wk after withdrawal of dox, showing strong correlation with reduced eosinophil levels. In contrast, IL-13-induced lung fibrosis did not significantly decline 4 wk after dox withdrawal. Importantly, IL-13-induced emphysema persisted, but modestly declined 4 wk after dox. Examination of transcript expression profiles identified a subset of genes that remained increased weeks after transgene expression was no longer detected. Notably, numerous IL-13-induced cytokines and enzymes were reversible (IL-6 and cathepsins), whereas others were sustained (CCL6 and chitinases) after IL-13 withdrawal, respectively. Thus, several hallmark features of IL-13-induced lung pathology persist and are dissociated from eosinophilia after IL-13 overexpression ceases.
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Registered trials
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.