Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Persistent effects induced by IL-13 in the lung.

Patricia C Fulkerson1, Christine A Fischetti, Lynn M Hassman

  • 1Department of Molecular Genetics, Biochemistry & Microbiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, 3333 Burnet Avenue, Cincinnati, Ohio 45229-3039, USA.

American Journal of Respiratory Cell and Molecular Biology
|April 29, 2006
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Genomic network analysis links uveitis with systemic inflammatory diseases.

medRxiv : the preprint server for health sciences·2026
Same author

Argon laser demarcation of AIDS-related cytomegalovirus retinitis in resource-limited setting.

International ophthalmology·2026
Same author

Peripheral blood markers of pediatric eosinophilic esophagitis.

The Journal of allergy and clinical immunology·2026
Same author

Longitudinal enrichment of eosinophilic esophagitis in children with AD: The MPAACH cohort.

The Journal of allergy and clinical immunology·2026
Same author

Comparison of PU.1 genomic binding across immune cells reveals cell type-specific roles in autoimmune disease.

medRxiv : the preprint server for health sciences·2026
Same author

COMPARISON OF PEDIATRIC PATIENTS WITH PARS PLANITIS WHO UNDERWENT TREATMENT VERSUS OBSERVATION AT A TERTIARY REFERRAL EYE CENTER.

Retina (Philadelphia, Pa.)·2026
Same journal

Correction to: Protective Role of Apelin in a Mouse Model of Post-Intensive Care Syndrome.

American journal of respiratory cell and molecular biology·2026
Same journal

Correction to: Sex-Specific Perinatal Nicotine-Induced Asthma in Rat Offspring.

American journal of respiratory cell and molecular biology·2026
Same journal

NF-κB-Dependent Transcriptional Regulation of Piezo1 Mediates Bacterial Clearance on Infected Lung Stiffness.

American journal of respiratory cell and molecular biology·2026
Same journal

Pathogenic Rewiring of IL6 Signaling Fuels Macrophage Immunometabolic reprogramming in COPD.

American journal of respiratory cell and molecular biology·2026
Same journal

Bridging the Gap: The Emerging Role of memory CD8+ T Cells in Fibrotic Interstitial Lung Disease.

American journal of respiratory cell and molecular biology·2026
Same journal

A Chimeric Airway Model Enables Evaluation of Essential Genes In Vivo.

American journal of respiratory cell and molecular biology·2026
See all related articles

Interleukin-13 (IL-13) overexpression causes lung inflammation and remodeling. While IL-13 levels decrease after stopping doxycycline, key pathologies like fibrosis and emphysema persist, indicating incomplete reversibility in asthma models.

Area of Science:

  • Pulmonary immunology
  • Respiratory disease research
  • Molecular biology

Background:

  • Interleukin-13 (IL-13) is a key driver of asthma pathogenesis, promoting inflammation and lung remodeling.
  • Current asthma therapies are often ineffective at reversing established lung structural changes.
  • Understanding the reversibility of IL-13-induced pathologies is crucial for developing better treatments.

Purpose of the Study:

  • To investigate the reversibility of lung pathologies induced by IL-13 overexpression.
  • To characterize the time course and extent of disease resolution after IL-13 withdrawal.

Main Methods:

  • Utilized a doxycycline-inducible transgenic mouse model for targeted lung IL-13 expression.
  • Administered doxycycline for 4 weeks to induce pathology, followed by withdrawal.

Related Experiment Videos

  • Assessed inflammatory cell infiltration, mucus metaplasia, fibrosis, emphysema, and gene expression profiles.

    • Main Results:

    • IL-13 withdrawal rapidly reduced IL-13 protein and eosinophils, but other inflammatory cells (macrophages, lymphocytes, neutrophils) remained elevated.
    • Mucus cell metaplasia significantly decreased, correlating with reduced eosinophils.
    • IL-13-induced lung fibrosis and emphysema showed limited reversibility, persisting weeks after IL-13 withdrawal.
    • Gene expression analysis revealed sustained upregulation of certain genes (e.g., CCL6, chitinases) despite reduced IL-13 levels.

    Conclusions:

    • Several key features of IL-13-induced lung pathology, including fibrosis and emphysema, are not fully reversible upon cessation of IL-13 overexpression.
    • Persistence of these pathologies is dissociated from eosinophil counts, suggesting complex resolution mechanisms.
    • These findings highlight the limitations of current therapies in reversing established lung remodeling in asthma.