More than 20 million Americans suffer from asthma, and children suffer in disproportionately high numbers. Scientists and doctors are working feverishly to find out exactly what causes the disease and how it can be cured, but there have not been any miracle findings yet. In 1872, a doctor discovered a type of white blood cell called eosinophils that is involved in inflammation and allergic diseases, such as asthma, which is most often triggered by allergens. Since then, the role of these cells has been debated; and still today no one knows if they are part of the cause of the disease or just an unwitting accomplice to the real culprit. Two new studies, one from the Mayo Clinic in Scottsdale, Ariz., and one from Harvard Medical School, use similar methods to report contradictory results—adding fuel to an already hot fire.

What the researchers wanted to know: What role do eosinophils play in asthma?

What they did: In both studies, the scientists genetically altered mice so that they did not have any eosinophils. However, they used different methods so that, though neither group of mice produced eosinophils, they were genetically different. In both studies, the scientists induced asthma in both normal and altered mice and compared the reactions of the two groups.

What they found: In the Mayo Clinic study, the authors found that the mice without eosinophils did not develop the hypersensitivity to airborne particles characteristic of asthma nor did they accumulate mucus in their lungs the way the genetically altered mice did. However, in the Harvard study, the mice without eosinophils didn't get off so easily. The genetically engineered mice were still hypersensitive to airborne particles and had similar amounts of mucus. However, the genetically engineered mice in this study did not develop changes in their airway that usually happen in asthma and were seen in the normal mice. (The Mayo Clinic study did not report on airway changes.) In a commentary on the two studies, immunologist Marsha Wills-Karp explains that two results could differ because the two populations of mice used in the studies have different genetic variations or because the mice used in the Mayo Clinic study may have been genetically engineered in a way that altered more than just their eosinophils.

What it means to you: Neither of these studies will quiet the debate about the role of these white blood cells in asthma. Because mice are genetically diverse, just like humans, it's likely that eosinophils play a larger role in the development of asthma for some people and not for others, says Wills-Karp, though no one has quite figured out what those roles are. The good news for asthma sufferers is that they are likely to inspire further studies that may eventually figure out what causes asthma and how it can be treated or prevented.

Caveats: The Mayo Clinic study engineered the mice in such a way that they might have altered some other, unknown biological function that could have inhibited the development of asthma in the mice. Also, because the studies contradict each other and other published studies, these studies don't lead to any final truths about the role of eosinophils in asthma.

Find out more: A general explanation of asthma, including its causes and potential triggers can be found on the Centers for Disease Control and Prevention website.

For people with asthma, one great resource is the daily pollen count, which gives pollen counts for cities around the country.

The National Institutes of Health has a definition of eosinophils, as well as an explanation of why they are tested in people with asthma.

Read the articles: Lee, J.J. et al. "Defining a Link With Asthma in Mice Congenitally Deficient in Eosinophils." Science. Sept. 17, 2004, Vol. 305, No. 5691, pp. 1773-1776.

Humbles, A.A. et al. "A Critical Role for Eosinophils in Allergic Airways Remodeling." Science. Sept. 17, 2004, Vol. 305, No. 5691, pp. 1776-1779.

Wills-Karp M. and Karp, C.L. "Eosinophils in Asthma: Remodeling a Tangled Tale." Science. Sept. 17, 2004, Vol. 305, No. 5691, pp. 1726-1729.

Abstracts online: Lee et al: www.sciencemag.org

Humbles et al: www.sciencemag.org