Pulmonary fibrosis is a mystifying disease that affects millions of people around the world. Researchers from the University of Illinois at Urbana-Champaign and Mei University studied pulmonary fibrosis and found a new bacterial protein fragment that initiates the death of lung tissues.
The study was led by professor Dr. Esteban Gabazza from Mei University and a microbiologist and animal sciences professor Isaac Cann from Illinois. The findings of the study are published in the journal Nature communications.
Isaac Cann said that salt-loving bacteria is found in the lungs of patients with pulmonary fibrosis and bacteria release a peptide molecule that marks the lungs cells for death.
After diagnosis within 5-6 years of life lung tissues become more stiffened and scarred in patients with pulmonary fibrosis. There are certain factors that are involved in the onset of diseases such as environmental factors, medication or infection. Several cases were found to have an unknown origin. These enigmatic cases are known as idiopathic pulmonary fibrosis (IPF). According to IPF Foundation, approximately 50,000 patients die every year in the U.S due to IPF. The ratio of death due to IPF is more as compared to the deaths due to breast cancer.
The progression of the disease is slow. The patient reaches a point where he experiences a fast worsening of breathing and this leads to loss of lung function. This phase is known as Acute exacerbation. The triggering cause for an acute exacerbation is still unknown.
Gabazza said that more than half of cases with IPF died due to acute exacerbation. The 50 percent of patients who survive after suffering from the acute exacerbation will live for more than 4 months.
Previous studies had shown that the proliferation of some bacteria such as certain strains of Staphylococcus, streptococcus, and Halomonas was found in the lungs of patients with IPF. This is because there was a high level of salt deposited in the lining of the lungs. Scientists cultured the bacteria in a lab that is linked with fibrotic tissue for studying what actually bacteria releases for triggering the acute exacerbation.
Researchers found a substance named a corisin as an exacerbating culprit. Gabazza’s group carried out an experiment on mice who have IPF. They compare the different samples of mice such as those mice given corisin itself, those who were infected with staph. strain and didn’t release corisin, those who were infected with corisin secreting staph. Nepalensis and untreated control group. They found that mice who were given corisin or those with bacterium infection secretions are at a greater risk of acute exacerbation.
Researchers also examined the human samples and found that patients with acute exacerbation have a greater level of corisin in their lung tissues.
Cann’s group explored the genome of staph. Nepalensis to know the site from where the corisin is secreted. A fragment of a large protein called peptide that triggers the corisin secretions in the lungs. A larger protein was also tested on the lung tissue to check whether it secretes the corisin or not, but scientists found no destructive properties similar to a small fragment
Researchers are now trying to find out the enzyme that cut the corisin from the large molecule of the proteins. This will help to block the activity of the enzyme to prevent the patients from acute exacerbation. They are also planning to identify the other strains of bacteria which release the corisin or small peptide. They also want to study the role of corisin and other bacterial strains in different types of fibrosis such as in liver and kidney.
Through knowing the cause of acute exacerbation, scientists will able to find out the way for fighting against it. This discovery could lessen the psychological stress of fighting against an unknown cause in the patients. On the other hand, it also compels the physicians to develop the treatments and drugs for this disease.