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In experiments, protective natural killer T (NKT) cells transplanted from mice exposed to a H. pylori glycolipid (P157) were enough to protect the lungs of other mice (below) against bronchial inflammation (above, purple and red stain).
Images courtesy of Ya-Jen Chang. |
In research that suggests a new strategy to prevent asthma, scientists in Children's Hospital Boston's Division
of Immunology and their colleagues have identified a mechanism by which certain infections in young children might shape their immune systems in a way that protects them from developing allergic asthma.
The study, published online December 13 by the Journal of Clinical Investigation, shows that exposing very young mice to influenza A infection protected them from developing airway hyperreactivity, a hallmark of asthma, as adults. Intriguingly, treatment with a glycolipid compound isolated from Helicobacter pylori had the same protective effect. The findings provide an immunologic mechanism in support of the "hygiene hypothesis," adding to evidence from epidemiologic studies associating certain childhood infections, such as respiratory viral infections or gastrointestinal H. pylori infection, with a lower risk for asthma.
In mice, influenza A infection appeared to confer its benefits by expanding
an immature cell type in the lung known as natural killer T (NKT) cells. Several
NKT-stimulating molecules known as glycolipids, including one isolated from
H. pylori, also expanded these cells in
the lung.
"Treatments focused on specifically expanding this inhibitory subset of cells in children might prevent the development of asthma," says senior investigator Dale
T. Umetsu, MD, PhD. "If we can understand how infections prevent asthma, we may be able to replicate the good parts and avoid the bad parts of infection."
Previous work by Dr. Umetsu's team implicated NKT cells—among the first responders to many infections—as a cause of asthma. In contrast, the new study, led by Ya–Jen
Chang, PhD, describes a subset of inhibitory NKT cells that seem to prevent allergic reactions in the airways—if stimulated at the right time by the right infectious agents or the right glycolipid.
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