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Antiviral protein in lungs may hold key to future asthma treatments

People with asthma produce less of an antiviral protein interferon-lambda (IFN-l) in response to rhinovirus infection than people without asthma, researchers have found.

Led by Sebastian Johnston from Imperial College London, the researchers aimed to find out whether the amount of IFN-l produced in people’s lungs affects their susceptibility or response to infection with rhinovirus, and whether their findings are different for asthmatic subjects.

They discovered that, in volunteers inoculated with rhinovirus, IFN-l production was inversely proportional to severity of symptoms, bronchoalveolar lavage virus load and airway inflammation (measured in bronchial lavage and sputum). Rhinovirus replication in primary bronchial epithelial cells was elevated in asthmatic compared with normal subjects.

Although incubation of bronchoalveolar lavage cells from rotavirus-infected subjects induced IFN-l production, this production was markedly impaired in those subjects who were asthmatic. The expression of mRNAs encoding for IFN-ls was also impaired in asthmatic compared with normal subjects.

The study does not shed light on whether IFN-l deficiencies are a cause of asthma or a consequence of the disease.

The researchers say: “The data identify a previously unknown mechanism of increased susceptibility to infection in asthma that is independent of steroid therapy, and suggest replacement of or augmentation of IFN-l production as new approaches to treatment or prevention of asthma exacerbations.”

The study is published online in Nature Medicine (13 August 2006).

Citation: The Pharmaceutical Journal URI: 10001925

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