Rogue gene linked to child asthma

21 November 2013 09:25

Scientists have discovered a rogue gene which could be a direct cause of severe asthma in young children

Scientists have discovered a rogue gene which could be a direct cause of severe asthma in young children

Scientists in the United States have discovered a rogue gene which could be a direct cause of severe asthma in young children.

They believe the discovery could lead to more effective, targeted treatments for severe, recurrent childhood asthma.

The team, led by Hakon Hakonarson of the Children's Hospital of Philadelphia (Chop), published its findings in the journal Nature Genetics.

The novel gene, CDHR3, was one of four identified as being associated with asthma, three of which were already known.

It was found to be especially active in epithelial cells lining the inner surfaces of the airways.

Suspect mutant versions of CDHR3 may cause abnormalities in the airway cell lining leading to an allergic response to environmental triggers.

Dr Hakonarson said the study concentrated on a specific phenotype - severe, recurrent asthma occurring between ages two and six - because asthma is a complex disease, with multiple interacting causes.

Identifying a risk-susceptibility gene linked to this phenotype may lead to more effective, targeted treatments for this type of childhood asthma, he said.

The US scientists made the discovery by comparing the genomes of 3,695 Danish children and adults, including a number of asthma sufferers two between two and six. Sufferers travelling abroad are advised to take out asthma travel insurance before embarking on their journey.

The latest findings - replicated using data from other children of both European and non-European ancestry - were consistent with previous research by Chop's Centre for Applied Genomics. They suggest other genes linked to childhood asthma play a role in over-sensitive immune reactions.

Asthma researchers have been increasingly interested in the role of the airway epithelium in the development of asthma, said lead researcher Dr Hakonarson.

He said abnormalities in the epithelial cells may increase a patient's risk to environmental triggers by exaggerating immune responses and making the airway overreact.

Because the CDHR3 gene is related to a family of proteins involved in cell adhesion and cell-to-cell interaction, "it is plausible that variations in this gene may disrupt normal functioning in these airway cells, and make a child vulnerable to asthma," he added.

But Dr Hakonarson cautioned that further studies were required to improve understanding of how the CDHR3 gene functions in asthma and develop new treatments for children most severely affected by the disease.

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