This chapter summarizes the current state of knowledge regarding the development and pathomechanism of inflammatory bowel disease (IBD) and describes the typical clinical presentation. IBDs are multifactorial diseases with no single cause. They are characterized by an excessive and unregulated inflammatory response that predominantly occurs in the intestines. The course is chronic—potentially lifelong—and typically progresses in flares. Numerous genetic alterations have been found that predispose individuals to developing IBD. Many of them are related to immune signalling pathways and the interaction between the immune system and gut bacteria. Against this background, external factors or environmental influences seem to promote the development of IBD. These include a Western lifestyle (especially a diet high in ultra-processed, low-fibre foods), use of antibiotics, and, in Crohn’s disease (CD), smoking. The microbiota (the collective microorganisms in the gastrointestinal tract) of IBD patients shows reduced diversity and altered function (dysbiosis). Another important factor in disease development is the increased permeability of the mucosal barrier in the gastrointestinal tract, which facilitates contact between gut antigens and the immune system. This ultimately results in an excessive activation of the immune system, involving various cell types and messengers from both the innate and adaptive immune systems. The mechanisms leading to an imbalance of these inflammatory responses in IBD are increasingly understood in detail and are addressed by modern targeted medications. CD is further characterized by the potential development of fibrotic tissue (fibrosis). IBDs are seen as a continuum of diseases that, in terms of localization, encompass at least three entities: (1) CD of the ileum, (2) CD of the colon, and (3) ulcerative colitis (UC). UC affects only the colon in varying degrees and is confined to the mucosal layer. CD, on the other hand, can affect any part of the intestinal tract and is characterized by transmural inflammation, which can lead to stenosis and fistulae. This results in different clinical manifestations. Although the intestine is the primary site of IBD, other parts of the body can also be affected (extraintestinal manifestations). IBD shares similarities with other immune-mediated infectious diseases. This chapter provides a basic understanding of the development of IBDs. This knowledge is helpful in everyday practice for taking patient history and advising patients with IBD and enables a better understanding of diagnostic and therapeutic strategies. It becomes clear that current treatments for IBD are not causal therapies and do not offer a cure. The information in this chapter facilitates the understanding of currently used drug therapies, which aim to suppress the inflammatory cascade (primarily monoclonal antibodies). Despite the wealth of detailed knowledge, some causal relationships remain the subject of further research, particularly the interaction between diet, microbiome, and the intestinal barrier.

Aetiology, Mechanisms of Disease and Clinical Picture

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发表日期：

2025年

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Michael Böhmig

摘要

This chapter summarizes the current state of knowledge regarding the development and pathomechanism of inflammatory bowel disease (IBD) and describes the typical clinical presentation. IBDs are multifactorial diseases with no single cause. They are characterized by an excessive and unregulated inflammatory response that predominantly occurs in the intestines. The course is chronic—potentially lifelong—and typically progresses in flares. Numerous genetic alterations have been found that predispose individuals to developing IBD. Many of them are related to immune signalling pathways and the interaction between the immune system and gut bacteria. Against this background, external factors or environmental influences seem to promote the development of IBD. These include a Western lifestyle (especially a diet high in ultra-processed, low-fibre foods), use of antibiotics, and, in Crohn’s disease (CD), smoking. The microbiota (the collective microorganisms in the gastrointestinal tract) of IBD patients shows reduced diversity and altered function (dysbiosis). Another important factor in disease development is the increased permeability of the mucosal barrier in the gastrointestinal tract, which facilitates contact between gut antigens and the immune system. This ultimately results in an excessive activation of the immune system, involving various cell types and messengers from both the innate and adaptive immune systems. The mechanisms leading to an imbalance of these inflammatory responses in IBD are increasingly understood in detail and are addressed by modern targeted medications. CD is further characterized by the potential development of fibrotic tissue (fibrosis). IBDs are seen as a continuum of diseases that, in terms of localization, encompass at least three entities: (1) CD of the ileum, (2) CD of the colon, and (3) ulcerative colitis (UC). UC affects only the colon in varying degrees and is confined to the mucosal layer. CD, on the other hand, can affect any part of the intestinal tract and is characterized by transmural inflammation, which can lead to stenosis and fistulae. This results in different clinical manifestations. Although the intestine is the primary site of IBD, other parts of the body can also be affected (extraintestinal manifestations). IBD shares similarities with other immune-mediated infectious diseases. This chapter provides a basic understanding of the development of IBDs. This knowledge is helpful in everyday practice for taking patient history and advising patients with IBD and enables a better understanding of diagnostic and therapeutic strategies. It becomes clear that current treatments for IBD are not causal therapies and do not offer a cure. The information in this chapter facilitates the understanding of currently used drug therapies, which aim to suppress the inflammatory cascade (primarily monoclonal antibodies). Despite the wealth of detailed knowledge, some causal relationships remain the subject of further research, particularly the interaction between diet, microbiome, and the intestinal barrier.