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Could bronchial asthma be an endogenous, pulmonary expression of retinoid intoxication?
1College of Health Sciences, Des Moines University-Osteopathic Medical Center, 3200 Grand Avenue, Des Moines, Iowa 50312, USA. anthony.mawson@dmu.edu
Insights
Childhood infections may protect against asthma by modulating immune responses. Lack of these infections might lead to retinoid buildup in the lungs, causing asthma exacerbations.
Area of Science:
- Immunology
- Pulmonology
- Nutritional Science
Background:
- Asthma prevalence has significantly increased in children over the past 30 years.
- Childhood infections are inversely associated with the development of atopy and asthma.
- The shift in CD4 T lymphocyte helper cells from Th2 to Th1 is a potential mechanism.
Purpose of the Study:
- To explore the potential role of retinoids in asthma development.
- To hypothesize a mechanism linking childhood infections, retinoids, and asthma.
Main Methods:
- Literature review and synthesis of existing research.
- Formulation of a novel hypothesis based on current evidence.
Main Results:
- The absence of certain childhood infections may lead to retinoid accumulation in the lungs.
- Retinoid metabolites, upon asthma trigger exposure, could cause localized intoxication.
Conclusions:
- Retinoid accumulation and subsequent intoxication are conjectured as a potential mechanism for status asthmaticus.
- Further research is needed to validate the proposed role of retinoids in asthma pathogenesis.
Abstract:
Asthma has become a major public health problem, affecting about 17 million people in the United States, including 4.8 million children. A striking increase in asthma and other forms of atopy has occurred in children in the U.S. and other western countries during the past 30 years. Several studies have reported an inverse association between childhood infectious illness and the development of atopy, suggesting that certain forms of infection protect against and even inhibit asthma. This may involve a shift in the balance of CD4 T lymphocyte helper cells from a Th2 to a Th1-type cytokine profile. However, the underlying mechanisms remain uncertain. Based on a review of the literature, it is conjectured that in the absence of certain types of childhood infection, retinoids (vitamin A and its congeners) accumulate in the lung. Later, upon exposure to known triggers for asthma, retinoid metabolites may be produced in such high concentration that they produce an acute, localized form of retinoid intoxication, recognized as status asthmaticus.