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Updated: Feb 26, 2026

Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Effects of β-blockers on house dust mite-driven murine models pre- and post-development of an asthma phenotype
Radhika Joshi1, Daniel Valdez1, Hosu Kim1
1Department of Pharmacological and Pharmaceutical Sciences, University of Houston, 3455 Cullen Blvd., Houston, TX 77204-5027, USA.
Background:
Our previous studies suggested certain β-adrenoceptor blockers (β-blockers) attenuate the asthma phenotype in ovalbumin driven murine models of asthma. However, the ovalbumin model has been criticized for lack of clinical relevance.
Methods:
We tested the non-selective β-blockers, carvedilol and nadolol, in house dust mite (HDM) driven murine asthma models where drugs were administered both pre- and post-development of the asthma phenotype. We measured inflammation, mucous metaplasia, and airway hyper-responsiveness (AHR). We also measured the effects of the β-blockers on extracellular-signal regulated kinase (ERK 1/2) phosphorylation in lung homogenates.
Results:
We show that nadolol, but not carvedilol, attenuated inflammation and mucous metaplasia, and had a moderate effect attenuating AHR. Following HDM exposure, ERK1/2 phosphorylation was elevated, but the level of phosphorylation was unaffected by β-blockers, suggesting ERK1/2 phosphorylation becomes dissociated from the asthma phenotype.
Conclusion:
Our findings in HDM models administering drugs both pre- and post-development of the asthma phenotype are consistent with previous results using ovalbumin models and show differential effects for nadolol and carvedilol on the asthma phenotype. Lastly, our data suggest that ERK1/2 phosphorylation may be involved in development of the asthma phenotype, but may have a limited role in maintaining the phenotype.
Insights
Nadolol, a beta-blocker, reduced airway inflammation and mucus in house dust mite asthma models, unlike carvedilol. This suggests differential effects of beta-blockers on asthma, with ERK1/2 phosphorylation potentially involved in its development.
Area of Science:
- Pulmonary Medicine
- Pharmacology
- Immunology
Background:
- Previous studies indicated beta-adrenoceptor blockers (β-blockers) could mitigate asthma in ovalbumin mouse models.
- The clinical relevance of ovalbumin-induced asthma models has been questioned.
Purpose of the Study:
- To investigate the effects of non-selective β-blockers, carvedilol and nadolol, on house dust mite (HDM)-induced asthma in mice.
- To assess the impact of β-blockers administered before and after asthma phenotype development.
- To explore the role of extracellular-signal regulated kinase (ERK 1/2) phosphorylation in asthma.
Main Methods:
- Utilized house dust mite (HDM) driven murine asthma models.
- Administered carvedilol and nadolol pre- and post-asthma phenotype development.
- Measured airway inflammation, mucous metaplasia, airway hyper-responsiveness (AHR), and ERK 1/2 phosphorylation.
Main Results:
- Nadolol, but not carvedilol, attenuated inflammation and mucous metaplasia in HDM-induced asthma.
- Nadolol demonstrated a moderate effect in reducing airway hyper-responsiveness (AHR).
- ERK 1/2 phosphorylation increased post-HDM exposure but was not affected by β-blocker treatment, suggesting dissociation from the established asthma phenotype.
Conclusions:
- Findings in HDM models align with previous ovalbumin model results, showing distinct effects of nadolol and carvedilol on the asthma phenotype.
- Data suggest ERK 1/2 phosphorylation is involved in asthma phenotype development but plays a limited role in its maintenance.
- The study highlights differential therapeutic potential of β-blockers in managing asthma.
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