Researchers in the United States and Japan say they have identified a bacterial protein fragment that appears to play a direct role in pulmonary fibrosis, a progressive lung disease that can scar healthy tissue and impair breathing.
In a study published in Nature Communications, scientists at the University of Illinois Urbana-Champaign and Mie University reported that corisin infiltrates lung cells, disrupts their protein quality-control system and triggers oxidative stress, premature cellular aging, cell death and scarring. The team said blocking corisin with an antibody reduced damage in laboratory experiments and improved survival in mice.
Evidence from patient samples and animal models
The researchers analyzed fluid collected from the lungs of patients with pulmonary fibrosis in Japan and compared it with samples from healthy volunteers. They found corisin-related bacterial DNA in the lung fluid, which they said was the first evidence that bacteria capable of producing the peptide were present in the lungs.
When the team removed corisin from patient samples using a custom antibody, the treated fluid lost its lethal effects on healthy cell cultures. The authors said this showed the peptide was biologically active and able to directly damage lung cells.
A potential new therapeutic target
To test whether corisin could drive disease on its own, the researchers engineered mice to continuously produce the peptide in their lungs. The animals developed pulmonary fibrosis spontaneously. When treated with the corisin-binding antibody, they showed reduced fibrosis, lower disease severity and improved survival.
Isaac Cann, an animal sciences professor at Illinois who co-led the study with Mie University immunology professor Esteban Gabazza, said the work moves corisin from an intriguing bacterial peptide associated with fibrosis to a mechanistically defined driver of disease and a possible therapeutic target. The team said it now plans to refine antibody-based approaches and explore additional strategies aimed at restoring protein quality or protecting mitochondria.
While the findings are early, the authors argued they provide proof of concept that neutralizing corisin could open a new route for treating pulmonary fibrosis and possibly other fibrotic diseases. The study was supported by multiple Japanese and U.S. research bodies, including the Japan Science and Technology Agency and the Japan Agency for Medical Research and Development.
For clinicians and researchers, the result adds to growing interest in how bacterial products may influence chronic disease far beyond infection. If confirmed in further studies, the discovery could help shift pulmonary fibrosis research toward interventions that target the disease process at a molecular level.
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