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Major Gene Link Seen to Childhood Asthma

A newly-discovered gene boosts the risk of childhood asthma by as much as 70 percent, according to an investigation into asthma-prone infants in five countries .

The culprit gene, called ORMDL3, is located on Chromosome 17, the paper, published online on Wednesday by the British science journal Nature, says.

Twenty-four experts from Britain, France, Germany, the United States and Austria joined the DNA trawl, comparing samples from 994 children with asthma against those from 1,243 local children who did not have the disease.

Asthmatic youngsters were between 60 and 70 percent likelier to have telltale mutations, called single-nucleotide polymorphisms, in their ORMDL3 gene than healthy counterparts.

"We are confident that we have discovered something new and exciting about childhood asthma," said Miriam Moffatt, from the National Heart and Lung Institute at London's Imperial College.

"These novel findings do not explain completely how asthma is caused, but they do provide a further part of the gene-environment jigsaw that makes up the disease."

In evolutionary terms, ORMDL3 appears to be a very old part of the human genome. Similar genes are found in primitive organisms such as yeast.

It may be a relic of some ancient human immune system, although its precise function -- and the role it appears to play in asthma -- remain unclear, said co-author William Cookson.

Asthma is an inflammation of the bronchial airways that causes the airways to constrict, causing shortness of breath and wheeziness.

The causes are complex, rooted in genetic susceptibility and in an allergic response to so-called environmental factors, such as air pollution, tobacco smoke, stress, strong emotions or exercise.

The disease has surged in prevalence in recent decades, especially in urban areas with poor air quality, and is now the commonest chronic disorder in childhood today. It is controllable, using drugs, but not presently curable.

"(ORMDL3) does not seem to be part of the allergic process," said Cookson. "As its expression is increased in asthmatics, it may be possible to develop therapies against it, but this will take time."


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