Scientists from Rutgers University found that obesity changes how airway muscles function, which increases the risk of developing asthma.
The research is published in the Journal of Physiology—Lung Cellular and Molecular Physiology and was conducted by Reynold Panettieri Jr. et al.
The prevalence of asthma and obesity—as both separate and coexisting conditions—has grown considerably in the United States in recent years.
Obesity is a major risk factor for asthma, in part, because of the systemic and localized inflammation of the airways that occurs in people with a high body mass index.
People with obesity also manifest a higher risk of severe asthma, decreased disease control, and decreased response to corticosteroids therapy.
Previous studies suggest that some people with obesity may have a type of asthma that is not caused by airway inflammation, but by hyper-responsiveness—a higher-than-normal response to an allergen—in the airway smooth muscle.
Hyper-responsiveness causes the airways to narrow, obstructing ease of breathing, and can occur when the muscles contract or begin to spasm.
In the new study, the team combined human airway smooth muscle cells with histamine, a chemical the immune system makes in response to an allergen, and carbachol, a drug that stimulates the part of the nervous system that controls the airways.
Stimulating airway cells with these substances causes the cells to release calcium, which mimics muscle contraction.
The team found that muscle cells from obese donors released more calcium and had greater shortening—a function that occurs during muscle contraction—than the cells from normal-weight donors.
Further, the cells from female obese donors released more calcium than cells from male obese donors.
The results suggest that obesity makes a unique and identifiable mark on the airway smooth muscle cells, which can lead to new ways to improve asthma management without the use of steroids.
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