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Updated: Jul 27, 2026

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Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
CCSP modulates airway dysfunction and host responses in an Ova-challenged mouse model
S Z Wang1, C L Rosenberger, T M Espindola
1Asthma and Pulmonary Immunology Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87185, USA.
Summary
Clara cell secretory protein (CCSP) deficiency exacerbates allergic airway disease in mice, increasing airway reactivity and inflammation. This highlights CCSP
Area of Science:
- Pulmonology
- Immunology
- Allergy Research
Background:
- Clara cell secretory protein (CCSP) is produced in the lungs and influences inflammatory responses to infection.
- The role of CCSP in allergic airway inflammation remains to be fully elucidated.
Purpose of the Study:
- To investigate the function of CCSP in the host's reaction to allergic airway disease.
- To determine if CCSP deficiency impacts airway hyperresponsiveness and inflammation in a mouse model.
Main Methods:
- CCSP-deficient (CCSP-/-) and wild-type (CCSP+/+) mice were sensitized and challenged with ovalbumin (Ova) aerosol.
- Airway reactivity, inflammatory cell counts (neutrophils), enzyme activity (myeloperoxidase), and cytokine levels (macrophage inflammatory protein-2) were assessed.
- Lung histopathology and mucus production were evaluated after Ova challenge.
Main Results:
- CCSP-/- mice exhibited significantly increased airway reactivity compared to wild-type mice following Ova challenge.
- Elevated neutrophil infiltration, myeloperoxidase activity, and macrophage inflammatory protein-2 levels were observed in CCSP-/- mice.
- Increased lung inflammation and mucus production were evident in the airways of CCSP-/- mice.
Conclusions:
- CCSP plays a protective role in modulating airway reactivity and inflammation during allergic airway disease.
- CCSP deficiency exacerbates allergic responses, suggesting CCSP is crucial for host defense in the airways.
- These findings underscore the importance of the airway epithelium in regulating responses to allergic inflammation.

