British scientists have identified a sequence of biological events that could trigger life-threatening asthma attacks in people suffering from colds – a finding that holds the potential for developing more effective medicines.
In a study published in the journal Science Translational Medicine, the researchers found that a small molecule, or ‘cytokine,’ called IL-25 may play a central role in the effect that viruses causing colds have on people with asthma.
According to the World Health Organization, 235 million people suffer from asthma worldwide and the condition is the most common chronic disease among children.
Viruses that infect the airways are the most common cause of asthma attacks, accounting for 80 to 90 percent of cases. Most of these are rhinoviruses, which are also the main cause of common colds.
Although illnesses caused by rhinoviruses are usually relatively mild for most people, they can also infect the lungs and, in people with respiratory conditions like asthma, can trigger severe attacks, sometimes leading to hospitalization.
“Our research has shown … that the cells that line the airways of asthmatics are more prone to producing a small molecule called IL-25, which then appears to trigger a chain of events that causes attacks,” said Nathan Bartlett, an expert at the Imperial College London’s national heart and lung institute who co-led the study.
He said that by finding a drug to target the molecule at the top of the cascade, “we could potentially discover a much-needed new treatment to control this potentially life-threatening reaction in asthma sufferers.”
Bartlett explained that the main features of an asthma attack – including inflamed and obstructed airways and increased mucus – are part of type-2 immune responses, which are more often seen in allergies and parasitic infections.
Until now, he said, it has been unclear how a rhinovirus infection can trigger these responses. But this study showed that IL-25 is induced by rhinovirus infection and is capable of instigating the production of other type-2 cytokines, creating a ‘cascade’ that drives the type-2 immune response.
The hope is that if scientists can target and block IL-25, this will stop the cascade and its consequences.
Professor Sebastian Johnston, also of Imperial who co-led the work, said existing asthma drugs containing inhaled steroids were highly effective at controlling regular asthma symptoms but that those suffering from a cold during an attack could see a worsening of their symptoms and end up in hospital.
He said the new results pointed to potential ways to address this big unmet medical need.
“The next steps are to test blocking IL-25 in humans and to investigate other possible pathways that could be important in asthma attacks and pool this knowledge to develop effective treatments,” he said.