Scientists have identified a bacterial protein fragment called corisin as a direct driver of pulmonary fibrosis, a finding that may help explain how scar tissue develops in the lungs and point to new treatment strategies. In a new study from the University of Illinois Urbana-Champaign and Mie University in Japan, researchers showed that corisin infiltrates cells, disrupts their quality-control system and triggers the chain of damage that leads to fibrosis. Blocking the fragment with an antibody reduced that harm.
What the researchers found
The team said corisin is not just associated with fibrosis but is biologically active and causally linked to disease. According to the researchers, the fragment can be present in fluid taken from the lungs of people with pulmonary fibrosis, and corisin-related bacterial DNA was also detected in those samples. When the scientists removed corisin with an antibody they developed, the fluid lost much of its lethal effect on healthy cell cultures.
The study also traced how corisin damages cells. Once inside lung cells, the fragment accumulates in mitochondria, where it disrupts protein quality control. That process then leads to oxidative stress, premature cellular aging, cell death and scarring. In mice engineered to continuously produce corisin in their lungs, pulmonary fibrosis developed even without an external bacterial source.
Why the discovery matters
The researchers said the work moves corisin from an intriguing bacterial peptide to a mechanistically defined target with therapeutic potential. Fibrosis can affect the lungs, kidneys, liver, heart, skin and other organs, and it contributes to nearly half of all deaths in developed countries, according to the study summary. The findings suggest that even very small amounts of native corisin may be enough to cause major biological effects.
Isaac Cann, an animal sciences professor at the University of Illinois Urbana-Champaign, said neutralizing corisin with the antibody largely protected cells from injury. Esteban Gabazza of Mie University added that the experiments showed corisin is remarkably potent and directly relevant to human disease.
The study adds to a growing body of life sciences research focused on the microbiome and on how microbial products may influence chronic disease. If further work confirms these findings in broader patient groups, corisin could become a target for future therapies aimed at slowing or preventing lung scarring.
Source: News-Medical report on the study
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