A faulty immune reaction - where the body reacts to non-existent parasites - could trigger asthma, a study suggests.
Asthmatics were found to have high chitinase levels
Yale University scientists found high levels of an enzyme called chitinase, produced by the immune system, soar in mice with asthma-like disease.
The enzyme is linked to parasites because it breaks down chitin, found on the surfaces of parasites and insects.
Writing in Science, the researchers say their findings may lead to new ways of treating asthma.
In their study, the Yale team found that those mice not bred to have the asthma-like disease had far less chitinase.
Lung tissue from humans with asthma also showed high levels of chitinase. The enzyme was undetectable in tissue from people who did not have the disease.
Overproduction of the enzyme was found to depend on a protein in the immune system called interleukin-13.
Extra IL-13, common in the lungs of asthmatics, is thought to help spark asthma attacks.
In simple creatures, such as worms and flies, chitinase is thought to protect against parasitic invasion.
Humans possess around half a dozen chitinase genes, but it was believed these were simply evolutionary relics.
However, the Yale University research suggests they might be stirred into action in asthmatics.
Their findings support a theory about the origins of asthma, which suggested t it is sparked off by the body sensing parasites when none are there.
That, it is thought, sends the immune system into overdrive, producing inflammation in the airways and asthma attacks.
The Yale researchers, led by Dr Jack Elias say human chitinase could be a useful new target for anti-asthma
Matthew Hallsworth, research development manager at Asthma UK, said: "It has long been suspected that there are many similarities between the body's response to parasites and the development of allergic conditions such as asthma.
"Exciting results such as these provide clues that will help us to begin to unravel the complex processes involved in the inflammation of the airways."