It has not been clear until now how a rhinovirus infection triggers the inflammation typical of an asthma attack, where the airways become obstructed and mucus production increases.
World Health Organization (WHO) statistics show that about 235 million people worldwide have asthma. About 80-90% of asthma attacks are caused by infections of the airways, particularly by rhinoviruses, which are also the main cause of the common cold.
In people with asthma, an otherwise-mild illness caused by a rhinovirus can trigger potentially severe attacks that may require hospitalization.
However, it has not been clear until now how a rhinovirus infection triggers the inflammation typical of an asthma attack, where the airways become obstructed and mucus production increases - known as the type-2 immune response.
To try and answer this, UK-based researchers from the Medical Research Council & Asthma UK Centre in Allergic Mechanisms of Asthma at Imperial College London and King's College London examined cells taken from the lungs of people with asthma and from healthy volunteers.
The researchers found that when the lung cells were infected with a rhinovirus, the cells from people with asthma produced around 10 times as many IL-25 cytokines as the cells from healthy volunteers.
Investigating further, the team infected both asthmatic and healthy volunteers with a rhinovirus and studied the IL-25 response across the two groups. The researchers found that the asthmatic participants had a higher level of IL-25 in nasal secretions than the healthy volunteers.
Chain reaction of molecules drives the type-2 immune response
Next, they simulated asthma in mice and infected them with a rhinovirus. The results of the mouse study demonstrated that the increased IL-25 response is also associated with increases in levels of other cytokines.
The researchers found that it is this "cascade" of molecules that drives the type-2 response, which usually occurs in response to allergies and viral infections. In the mice, blocking IL-25 was an effective way to decrease the levels of the other cytokines.
These results, say the team, suggest that drugs targeting IL-25 in humans could form the basis of new asthma treatments.
Joint lead author of the study Dr. Nathan Bartlett, honorary lecturer at the National Heart and Lung Institute, Imperial College London, explains:
"Our research has shown for the first time 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. By targeting this 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."
The next step will be to attempt to block IL-25 in humans and investigate other pathways that may contribute to asthma attacks.
Dr. Samantha Walker, director of research and policy at Asthma UK, says that years of underfunding in asthma research means that the mechanisms behind the illness remain a relative mystery.
"Excitingly, this research, although still at an early stage, could potentially lead to the development of new medicines to prevent life-threatening asthma attacks," she says. "The millions of people with asthma need more studies like this to bring us one step closer to new treatments."