Crohn’s disease begins when immune command centres in the gut wall turn from defenders into attackers, creating small ulcers that spread into widespread inflammation. Around 190,000 people in the UK have the condition, with rising rates particularly among children, yet current treatments only work for some patients and many eventually need surgery. The problem is that scientists have not been able to study the earliest stages of inflammation directly in human tissue. This project will use new techniques to isolate immune cells from gut samples taken from patients, identifying exactly which cells and signals trigger the damaging response. A specially designed mouse model that mimics this early stage will then be used to test whether blocking those signals can prevent inflammation from spreading. If successful, this work could identify new targets for treatments that stop Crohn’s disease before it causes lasting damage to the gut wall. That would mean fewer patients relying on surgery and more people experiencing longer-lasting relief from pain and fatigue. The research is fundamental science, but understanding the precise chain of events that turns protective immune cells into destructive ones is the first step toward therapies that intervene earlier and more effectively.
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Crohn’s disease is a chronic inflammatory condition of the gut, causing severe pain, fatigue, and digestive problems. It affects approximately 190,000 people in the UK, with rising incidence, especially among children. Although genetics, environmental factors, and the immune response to gut bacteria are known to contribute to the disease, the precise reasons why inflammation starts and spreads throughout the gut remain poorly understood. This research focuses on specific areas within the gut known as Gut-Associated Lymphoid Tissues (GALT). These immune 'command centres' are normally involved in protecting the gut against harmful bacteria. However, in Crohn’s disease, GALT become overactive, leading to small ulcers and inflammation that spread to cause widespread damage to the gut wall. Current therapies mainly aim to suppress the resulting inflammation and are effective in only some patients, leaving the majority of patients requiring surgery when treatments fail. My project aims to address this major challenge by exploring how immune cells within GALT trigger inflammation in Crohn’s disease. Using recently developed techniques, I will isolate and study these immune structures directly from patient gut samples, something not previously possible. By examining the types and activities of immune cells present, this research aims to identify the key processes initiating inflammation. Additionally, current experimental animal models often fail to replicate key features of human Crohn’s disease, particularly the critical GALT-associated stage of inflammation. To overcome this limitation, I will use a mouse model specifically designed to mimic this aspect of the disease closely. This model will help validate findings from human tissue analysis and enable testing of new potential therapies to control or prevent gut inflammation. The combination of highly targeted human tissue data and innovative animal models will significantly enhance our understanding of Crohn’s disease. Ultimately, this research could identify new targets for treatments that are more effective and provide longer-lasting relief for patients, reducing reliance on surgery and improving quality of life.
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