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Vitamin A deficiency promotes bronchial hyperreactivity in rats by altering muscarinic M(2) receptor function
Stephen E McGowan1, Jennifer Smith, Amey Jo Holmes
1Department of Veterans Affairs Research Service, University of Iowa College of Medicine, Iowa City, Iowa 52242, USA. stephen-mcgowan@uiowa.edu
Insights
Vitamin A deficiency (VAD) in children increases respiratory infection mortality. VAD also promotes bronchial hyperreactivity by impairing the M2 receptor
Area of Science:
- Pulmonary Medicine
- Nutritional Science
- Respiratory Physiology
Background:
- Vitamin A deficiency (VAD) is a significant global health issue, particularly in developing nations.
- Children with VAD face higher mortality rates from respiratory infections.
- Bronchial hyperreactivity, a condition linked to asthma, can arise after viral respiratory infections.
Purpose of the Study:
- To investigate the potential link between VAD and the development of bronchial hyperreactivity.
- To assess the impact of VAD on methacholine-induced bronchoconstriction in a rat model.
Main Methods:
- Assessed methacholine-induced bronchoconstriction in rats with VAD and vitamin A-sufficient rats.
- Evaluated bronchial wall thickness and small molecule clearance.
- Measured the function and abundance of muscarinic M(2) receptors in bronchial tissue.
Main Results:
- VAD rats exhibited bronchoconstriction at lower methacholine concentrations compared to sufficient rats.
- This increased reactivity was not due to thickened bronchial walls or altered small molecule clearance.
- Reduced function and abundance of muscarinic M(2) receptors were observed in VAD rats.
Conclusions:
- VAD promotes bronchial hyperreactivity, potentially by impairing muscarinic M(2) receptor function.
- This finding suggests a role for vitamin A in regulating airway responsiveness, similar to its role in asthma.
- Vitamin A (retinol) and retinoids may be crucial for maintaining normal bronchial responsiveness and epithelial health.
Abstract:
Vitamin A deficiency (VAD) remains an important health problem among children in developing countries. Children living in these areas have a higher mortality from respiratory infections, which likely results in part from suboptimal nutrition, including VAD. Bronchial hyperreactivity can follow viral respiratory infections and may complicate the recovery. To investigate whether VAD promotes bronchial hyperreactivity, we have assessed methacholine-induced bronchoconstriction in VAD and vitamin A-sufficient rats. Bronchial constriction developed at lower concentrations of inhaled methacholine in VAD than in vitamin A-sufficient rats. This did not result from an increase in the bronchial wall thickness or the clearance of a small molecule (with a size similar to methacholine) from the air space. The function and abundance of the muscarinic M(2) receptors in bronchial tissue were reduced in VAD rats, suggesting that this receptor may contribute to these animals' diminished ability to limit cholinergic-mediated bronchoconstriction. A similar reduction in muscarinic M(2) receptor function has been observed in asthma. Vitamin A (retinol) and its congeners (retinoids) may be required to regulate bronchial responsiveness in addition to maintaining a normal bronchial epithelium.