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Researchers have known for years that one chemical that can 't exit cells because of the mutation in cystic fibrosis patients' CFTR is chloride. This resulted in the widespread use of the term "chloride channel" to describe the pathway that CFTR is supposed to form. Much former and current cystic fibrosis research looks at the question of why chloride's inability to exit cells causes the ill effects of the disease.

That's where Hudson's approach diverges from the status quo - her research holds that it is not chloride that is primarily responsible, but that another chemical trapped by the malfunctioning CFTR - glutathione - plays a crucial role. She noticed that the symptoms of individuals with a known deficiency of glutathione outside their cells are remarkably similar to the symptoms of cystic fibrosis patients. She then identified a chemical mechanism that explains that effect.

In healthy people, the cells lining the lungs, which are called epithelial cells, release glutathione onto the lungs' surface, where it performs several important functions. As is widely recognized by scientists, glutathione acts as an antioxidant that neutralizes harmful oxidants in the air and those released by immune system cells. The body also uses glutathione to break down mucus and make it thinner.

By the time they are in their teens, cystic fibrosis patients have between 5 and 20 percent of the levels of glutathione on the surface of their lungs that healthy people do. The defect in their CFTR protein prevents the chemical from exiting their epithelial cells. Therefore, the patient's lungs are more susceptible to damage from oxidants and are plagued with thicker mucus than healthy people's are.

Those damaging effects fit easily into Hudson's hypothesis, but extracellular glutathione deficiency at first did not easily explain why cystic fibrosis patients are chronically inflamed, even before becoming infected. Then she found research that showed that certain immune system cells have another protein channel beside CFTR that does allow glutathione to exit. She hypothesizes that, in a cystic fibrosis patient's glutathione-starved lungs, the immune system cells emit a significant amount of their glutathione in a futile attempt to make up the difference, rendering them weak and ineffective. Low levels of glutathione in immune system cells also signal inflammation. 

That leaves patients suffering from a vicious cycle - the lungs are chronically inflamed and laden with thick mucus, which harbors infections. The immune system cells that are marshaled to attack the infection are weakened and rendered less effective by a depletion of glutathione. This leads the body to summon more immune system cells that produce oxidants normally neutralized by glutathione but that instead ravage the lung surface. The immune system also produces by-products that build up, making the mucus even thicker.

Based on that biochemical mechanism, Hudson's solution is simple - restore glutathione in the lungs to a healthy level and halt the cycle.