Researchers have reported new evidence that a bacterial protein fragment called corisin may directly damage lung cells and drive pulmonary fibrosis, a progressive scarring disease that makes breathing increasingly difficult. The findings, published in Nature Communications, build on earlier work suggesting corisin could harm lung tissue, but now point more clearly to a local source in the lungs as well as a mechanism that could be targeted for treatment.
The team analysed fluid samples from patients with pulmonary fibrosis, including samples taken during acute worsening of the disease, and compared them with control samples from healthy volunteers. They found corisin-related bacterial DNA in the fluid, which they said was the first evidence that peptide-producing bacteria were present in the lungs. When they removed corisin from patient samples using an antibody they developed, the fluid lost its toxic effect on healthy cell cultures.
How corisin appears to damage the lungs
According to the researchers, corisin enters lung cells and accumulates in the mitochondria, where it disrupts the cell’s quality-control system. That process appears to trigger oxidative stress, premature cellular aging, cell death and scarring. The group also engineered mice to continuously produce corisin in their lungs, and those mice spontaneously developed pulmonary fibrosis without any outside bacterial source of the peptide.
When the mice were treated with the corisin-binding antibody, their fibrosis was significantly reduced, disease severity fell and survival improved. The researchers said these results provide proof of concept that neutralising corisin could become a new therapeutic strategy for pulmonary fibrosis and possibly other fibrotic diseases.
Why the findings matter
Pulmonary fibrosis is one form of tissue fibrosis, a process in which healthy tissue is replaced by scar tissue. The researchers noted that fibrosis can affect the lungs, kidneys, liver, heart, skin and other organs, and contributes to nearly half of all deaths in developed countries. While more work is needed before any treatment reaches patients, the study offers a potential path toward therapies that interrupt the disease earlier in its course.
The scientists said they plan to further refine the antibody approach and explore other strategies aimed at protecting mitochondria or restoring protein quality inside cells. For clinicians and patients facing pulmonary fibrosis, the work adds to growing interest in how microbial products and cellular stress pathways may interact in chronic disease.
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