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Related Experiment Video

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A Reversible, Non-invasive Method for Airway Resistance Measurements and Bronchoalveolar Lavage Fluid Sampling in Mice

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Understanding the pathogenesis of allergic asthma using mouse models.

K P Leong¹, D P Huston

¹Department of Rheumatology and Immunology, Tan Tock Seng Hospital, Singapore. khai_pang_leong@notes.ttsh.gov.sg

Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology

|August 31, 2001

Summary

Mouse models reveal allergic asthma pathogenesis, highlighting Type 2 T helper cells and multiple pathways driving airway hyperresponsiveness (AHR). These models also test novel asthma therapies.

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Area of Science:

Immunology
Allergy and Asthma Research
Translational Medicine

Background:

Allergic asthma is characterized by airway inflammation and hyperresponsiveness (AHR).
Understanding the underlying pathogenesis is crucial for developing effective treatments.

Purpose of the Study:

To review current views on the pathogenesis of airway eosinophilic inflammation and AHR in allergic asthma.
To explore new treatment strategies informed by mouse model research.

Main Methods:

Conducted MEDLINE searches using keywords: asthma, mouse model, murine.
Selected original research and review articles from peer-reviewed journals.
Identified additional relevant articles from references.

Main Results:

Mouse models, while not identical to human asthma, offer applicable insights into pathogenesis.
Type 2 T helper (Th2) lymphocytes are central to orchestrating inflammation and AHR.
Three key pathways contribute to AHR: IgE/mast cell-dependent, eosinophil/IL-5-dependent, and IL-13-dependent.
Eosinophils are identified as critical effector cells in AHR.

Conclusions:

Airway hyperresponsiveness (AHR) in asthma is driven by airway inflammation mediated by helper T cells through at least three distinct pathways.
Mouse models serve as valuable platforms for testing and developing novel asthma therapies.