Even short-lived, lung infections such as Covid-19 can lead to long-term sequelae, such as breathing difficulties. A team of researchers has just identified a protein involved in these lasting effects.
- Even after the virus is cleared from the body, the lungs can suffer damage that can develop into chronic lung disease.
- These lesions are due to the expression of a protein called IL-33 which, in the event of infection, is responsible for cell proliferation, the appearance of mucus and inflammation in the lungs.
Even when respiratory viruses like those responsible for Covid-19, pneumonia or bronchiolitis no longer affect the body, their harmful effects are still felt. Many patients suffer, for example, from a persistent cough, difficulty in breathing or shortness of breath on the slightest effort. In fact, the peak of respiratory disease often occurs within weeks of the virus being cleared, resulting in damage that can lead to chronic disease or, in the worst case, death.
For the first time, researchers at the Washington University School of Medicine in Saint Louis (USA) have shed light on the process behind the appearance of these lasting lung lesions. In a study published in the Journal of Clinical Investigation, they explain having discovered that the viral infection triggers the expression of a protein. Called IL-33, it is needed for lung stem cells to grow in the airspaces, but increases mucus production and inflammation in the lung when overexpressed.
Mucus and inflammation after the infection is over
Doctors have long known that acute respiratory infections can lead to chronic lung disease. However, until now they did not know how an acute respiratory infection triggers a chronic disease, making it difficult to develop therapies to prevent or treat it.
To find out, the researchers infected mice with the Sendai virus, an RNA virus that replicates in the respiratory tract of animals but does not cause serious illness in humans. They then examined lung tissue 12 and 21 days after infection, and compared the samples to lung tissue from uninfected mice.
They then found that in infected mice, stem cells divide and begin to produce mucus, while others release molecules that recruit immune cells to the lungs. This process results in lungs with less air space, more mucus and continued inflammation which together interfere with breathing.
The key role of the IL-33 protein
Other experiments carried out by the team showed that these lung lesions are due to the IL-33 protein. Normally, this essential protein helps lung stem cells repair virus damage, but it can also play a more detrimental role after infection, promoting cell proliferation, the appearance of mucus and therefore inflammation.
By suppressing the production of this IL-33 protein in the lungs of modified mice, the researchers found that 7 weeks after infection, the basal cells showed higher oxygen levels in the blood and less hyperresponsiveness of the airways. , two signs of improvement in their chronic lung disease.
The researchers hope that this discovery can form the basis of effective therapies to prevent or treat lung diseases caused by viruses.
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