Heart and lungs

Study finds clue to why colds trigger asthma

The Mail Online reports how "a simple cold can set off a deadly asthma attack: Scientists discover chemical can send the immune system into overdrive".

It is well known that in people with asthma, respiratory infections such as colds or flu can trigger asthma symptoms, and, in more serious cases, an asthma attack.

This study involved experiments in mice and humans to see exactly why this might be the case. In particular, the researchers wanted to find out how inflammatory processes might play a part.

They found in people with asthma, infection with the common cold virus (rhinovirus) causes an increase in levels of an inflammatory protein called IL-25 in the cells lining the airways.

This sets off a range of inflammatory processes, such as narrowing of the airways, which can cause asthma symptoms.

As the researchers suggest, the findings indicate using a drug to block IL-25 could prevent people with asthma getting worse symptoms if they catch a cold.

This research is in its early stages and further studies will now be needed to develop an IL-25-blocking drug for testing.

Where did the story come from?

The study was carried out by researchers from Imperial College London.

It was funded by the Medical Research Council, Asthma UK, the National Institute for Health Research, Imperial Biomedical Research Centre and the Novartis Institute for Biomedical Research.

The study was published in the peer-reviewed journal Science Translational Medicine.

The Mail Online's reporting of the study was accurate.

What kind of research was this?

This was laboratory, human and animal research that aimed to investigate the role a protein called interleukin-25 (IL-25) plays in triggering worsening symptoms in people with asthma when they catch a cold.

Viral infections such as the common cold (mostly caused by rhinoviruses) are known to be a trigger for worsening asthma symptoms or causing asthma attacks.

IL-25 is a protein involved in inflammatory and autoimmune processes (where the immune system attacks health tissue) in the body and has previously been identified as playing a role in asthma.

This study used laboratory experiments and studies in mice and humans. The results showed how people with asthma express more IL-25, and that infection with rhinovirus can increase levels of IL-25 and other inflammatory molecules.

What did the research involve?

The researchers first studied samples of the cells lining the airways in the lungs (the bronchi) obtained from 10 people with asthma and 10 people without asthma.

They looked at the levels of IL-25 and then looked at what happened when these cells were infected with rhinovirus.

They then followed up these laboratory results with studies in mice and humans. The researchers infected 39 people with rhinovirus – 28 people with asthma and 11 people without asthma – to see what effect this had on the levels of IL-25 in nasal secretions.

They then studied mice to look at the exact mechanisms by which rhinovirus may lead to increased IL-25 and so trigger asthma symptoms.

A mouse model of asthma was used in these experiments. In this model, the mice were sensitised with an allergen once daily for three days via the nose, while some were given a saline control.

The allergen used was RV-OVA, which causes allergic inflammation in the airways similar to that which occurs in people with asthma.

After this sensitisation, some were infected with rhinovirus, while some were not. The researchers then examined the levels of IL-25 and inflammatory cells in the airways. 

The researchers followed this up by investigating the effects of an IL-25-blocking antibody in mice.

What were the basic results?

In the first laboratory study, the researchers found the cells lining the airways in people with and without asthma were no different in how much IL-25 they produced when they were not infected with rhinovirus.

After eight hours of exposure to rhinovirus, infected cells showed tenfold greater levels of IL-25 than those not infected. Using allergy tests, the researchers found increased IL-25 expression was associated with increased sensitivity to various allergens.

Their next experiments in people both with and without asthma showed there was no significant difference in the level of IL-25 nasal secretions before rhinovirus infection.

Up to 10 days after infection with rhinovirus, 61% of those with asthma (17 of 28) demonstrated a significant increase in their IL-25 levels.

People without asthma also had a significant increase in IL-25 secretion, but peak levels during infection were higher in people with asthma.

The researchers found the "asthmatic mice" (whose airways had been sensitised by the allergen RV-OVA) had higher IL-25 levels, whether subsequently infected with rhinovirus or not, compared with the "non-asthmatic" mice.

When "allergic" mice were infected with rhinovirus, they had IL-25 levels 28 times higher than asthmatic mice who were not infected. Infection of non-asthmatic mice with rhinovirus also caused an increase in IL-25 levels compared with non-asthmatic, non-infected mice, but at much lower levels.

Further examination of lung tissue from the mice demonstrated the inflammatory response that was occurring in association with IL-25. Using an IL-25-blocking antibody blocked the inflammatory response in the mice's lungs that occurred after rhinovirus infection. 

How did the researchers interpret the results?

The researchers concluded that rhinovirus can induce IL-25 production in the lining of the airways, and that this is more pronounced in people with asthma than healthy controls.

In a mouse model of allergic asthma, rhinovirus infection induced IL-25 production, and blocking IL-25 could reduce rhinovirus-induced lung inflammation.


It is well known that respiratory infections such as colds or flu can trigger asthma symptoms in those who have the condition.

This study demonstrates how, in people with asthma, infection with the common cold virus (rhinovirus) causes an increase in levels of the inflammatory protein IL-25 in the cells lining the airways. This sets off an inflammatory process that could be causing the asthma symptoms.

As the researchers suggest, the findings indicate that using a drug to block IL-25 could be a promising way to try to prevent people with asthma getting worse symptoms if they catch a cold.

The research is in its early stages, and further studies will now be needed to develop an IL-25-blocking treatment that shows enough promise to be tested in human trials.

While there is no guaranteed way to prevent catching a cold, people can help prevent the spread of colds by always coughing or sneezing into a tissue, binning it and washing their hands.

NHS Attribution