“Our study establishes that fibrin is a powerful, although context-dependent, determinant of inflammatory joint disease,” said Jay Degen, Ph.D., a researcher in Developmental Biology at Cincinnati Children’s Hospital and the study’s lead author.
He an his team states that RA appears to be driven by the engagement of inflammatory cells with fibrin matrices through a specific integrin receptor, aMB2.
The study was conducted by a team that includes researchers from Cincinnati Children’s and the University of Cincinnati’s College of Medicine using genetically engineered mice with collagen-induced arthritis of the knee and paw. The mice were designed to have selective alterations in the production of fibrinogen, a precursor to fibrin, to allow researchers to evaluate the inflammatory impact of fibrin, especially as it interacts with aMB2.
The researchers suggest that therapies designed to interrupt the localized interaction of inflammatory cells and fibrin may help arthritis patients. “The findings also suggest that pharmacologically interrupting the interaction of fibrin and aMB2 might be efficacious in the treatment of arthritic disease as well as many other inflammatory diseases, such as multiple sclerosis,” Degen said.
Although the disease’s precise cause is not fully known, activation of specific components in the body’s immune system seem to play a major role in its onset and early progression, according to researchers. Fibrin deposits are a prominent feature of arthritic joints and the protein appears to be a link between systems that control inflammation and bleeding within joints. Degen and colleagues explained that in arthritic joints, the mesh-like matrices formed by fibrin to create blood clots may control local activity of inflammatory cells as well as support inappropriate tissue reorganisation.
MEDICA.de; Source: Cincinnati Children's Hospital Medical Center