This study finding an new pathway; to identify the potential treatment target for the Crohn’s disease. As there is no cure for the more than 1.6 million people in the people living with Crohn’s disease (CD) and its symptoms, including abdominal pain, intestinal distress and severe weight-loss. CD is a form of inflammatory bowel disease (IBD) in which the body’s own immune system attacks the gastrointestinal tract, and treatment is focused on controlling the symptoms of the disease in its acute phase and managing it in remission.
Potential treatment target
As Crohn’s disease (CD) is a debilitating inflammatory disorder that affects more than 1.6 million people in North America alone. Members of the tumor necrosis factor super family are key regulators of intestinal inflammation; specifically, tumor necrosis factor like weak inducer of apoptosis (TWEAK) and its receptor; fibroblast growth factor–inducible 14 (Fn14); are involving in normal and pathologic tissue remodeling. Our aim was to determine the role of TWEAK/Fn14 in CD and a murine model of CD-like ileitis.
But recently, researchers identifying a pathway in the immune system activating in Crohn’s disease (CD) and which holds promise for investigating new treatments. As the study investigating the interaction between a class of proteins called tumor necrosis factor and receptors on the surface, called Fn14. Their goal was to see how the tumor necrosis factor (or TWEAK, for Tumor Necrosis Factor-like Weak Inducer of Apoptosis) and its cell receptor; Fn14, may play a dual role of both protecting the intestine from acute and chronic inflammation characteristic in CD; and how it might also trigger it.
The chronic inflammation
But by studying the TWEAK/Fn14 interaction for at least two decades to understand its role in inflammation. Cominelli and his team, however, are the first to describe this signaling complex in CD. During early inflammation, TWEAK/Fn14 activates to heal tissue damage. However, during later, chronic inflammation; increased and persistent levels of Fn14 may lead to pathologic inflammation and fibrosis.
They also may cause hypertension, infection and the risk of birth defects in pregnant women being treated for IBD. As CD patients endure a roller-coaster ride of flare-ups, repeated hospital stays; surgeries and treatments relieved by intervals of remission, the disease becomes dramatically life-changing and emotionally stressful. To better understand the link between TWEAK/Fn14 and chronic inflammation, the team of researchers used mice bred to develop CD-like disease, and then genetically deleted the cell-surface receptor Fn14.