Abstract
While the prevalence of asthma and atopic disease continues to rise over the past half a century, the exact mechanism behind this remains elusive. Of late, the role of metabolic dysfunction in disease is becoming more clearly classified. The part of metabolic dysfunction in respiratory viral infections is studied, which reopens the debate in the role of infection on asthma development in childhood. During infection, there is a rapid shift in nutrients available for immune cells to metabolize. Exploring these metabolic changes and the resulting immune cell function, a striking pattern emerges. In asthma development following viral infection, it is proposed there is a transient state of impaired glucose tolerance resulting in a sudden increase in glucose for lymphocytes to metabolize, triggering them to enter a state of increased aerobic glycolysis. Reviewing this outcome, along with previous work, a new working metabolic model of asthma development is proposed by suggesting a new step between a healthy immune system and asthma.
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