Grant: Project Grant

Approximately 2-4% of Canadians have fibromyalgia, a syndrome characterized by wide-spread chronic pain, fatigue and cognitive difficulties. Despite its commonness fibromyalgia lacks diagnostic tests and pain management strategies are limited. Our recent studies suggest that a particularly painful subset of fibromyalgia is caused by autoantibodies. Why fibromyalgia autoantibodies develop, and what their precise targets are remains unknown. Our hypothesis is that fibromyalgia autoantibodies develop through a process called cross reactivity. Cross reactive autoantibodies can develop when gut microbes, like bacteria, stimulate an antibody producing immune response, and if those antibodies also recognize proteins in our own body, then an autoantibody response can develop. Our proposed work will investigate how fibromyalgia autoantibodies develop through cross-reactivity with gut bacteria and identify the bacteria to which the antibodies bind. We will then use computational and biochemical approaches to discover antibody targets that are similar between humans and bacteria. We will also use fecal microbiota transplants into mice to study autoantibody development and autoantibody induced pain behaviour. Finally, we will determine the role of different immune cells in the development of painful FM autoantibodies through cross-reactivity. The long-term goals of this research are to identify the bacterial and human targets of fibromyalgia autoantibodies and then develop diagnostic tests. Tests could divide fibromyalgia patients for already existing immunomodulatory treatments.