Author: Janis Weiss
Every year, more than 300,000 Americans contract Lyme disease, an infection caused by bacteria Borrelia burgdorferi transferred during a tick bite. Arthritis is one of the most common complications resulting from this infection. In a small percentage of patients, arthritis persists despite antibiotic treatment. Today, researchers are focusing on understanding the role of the immune system in controlling the range of arthritis severity that patients experience.
Previous work showed the role of the immune system in how arthritis develops. In particular, researchers identified the position on a gene of the type I interferon (IFN), a gene cluster triggered by a B. burgdorferi infection. When triggered, the cluster elicits a complex cascade of responses that drive Lyme arthritis severity. Using a mouse model, the researchers focused on two positions in the cluster — IFN-α and IFN-β. They identified IFN-b as the species responsible for controlling arthritis severity.
The researchers also found myostatin, a protein produced and released by muscle cells that inhibit muscle fibers, mediates the development of IFN-regulated Lyme arthritis. While the signaling pathways underlying inflammatory arthritis remain unclear, targeting myostatin offers an appealing therapy to the standard anti-inflammatory approach to suppress arthritis development.