Millions of adults live with inflammatory disorders affecting the gut, such as inflammatory bowel disease (IBD)—which includes Crohn’s Disease (CD) and ulcerative colitis—and ileitis, or inflammation of the ileum, which includes Crohn’s ileitis and CD-like ileitis. These diseases are characterized by chronic inflammation of the gastrointestinal tract, where an impaired mucosal barrier, dysbiosis, and disrupted communication between the innate immune system and commensal microflora can lead to painful symptoms. They are affected by environmental conditions, such as the balance of animal and plant protein sources in the patient’s diet, and by genetic factors, including polymorphisms in genes such as NOD2 and ATG16L1, which are involved in innate immunity, autophagy, and phagocytosis. The intersection of gut cells, immune cells, and the microbiota is clearly a critical communication axis and the junction through which errant signaling, including interleukins like IL-1, can lead to dysfunction and disease. The gut-associated lymphoid tissue that is spread throughout the intestine comprises a significant portion of the body’s immune system, and research shows that the human gut holds a large quantity of immune cells, including CD8+ T cells that can contribute to the tissue damage experienced in IBD. In this webinar, the speakers will discuss inflammatory disorders in which altered innate immune cell function leads to diseases such as CD-like ileitis and IBD, and potential ways to mitigate the mechanisms that drive this inflammation.
