Inflammatory bowel disease (IBD) refers to a group of chronic, nonspecific inflammatory disorders of the gastrointestinal tract with an unknown etiology. The main types include ulcerative colitis (UC) and Crohn's disease (CD).
Etiology and Pathogenesis
The exact cause of IBD remains unclear. Current research suggests that it results from an interplay of environmental, genetic, and gut microbiota factors, leading to immune dysregulation.
Environmental Factors
Over the past century, the global incidence of IBD has steadily increased, initially observed in economically developed regions such as North America and Europe.
Genetic Factors
IBD displays a genetic predisposition. The incidence in first-degree relatives of patients is significantly higher than in the general population, and the concordance rate in monozygotic twins is markedly higher than in dizygotic twins. Certain genetic mutations, such as those in the NOD2 gene, have been associated with IBD in Caucasian populations. However, no genes have been identified as closely linked to IBD in the Chinese population. This difference reflects variations in genetic backgrounds across different races and populations.
Gut Microbiota
Patients with IBD exhibit dysbiosis of the gut microbiota, characterized by reduced microbial abundance and diversity. Experimental animal models of IBD constructed using gene-engineering techniques require the presence of gut microbiota to trigger an inflammatory response, highlighting the critical role of gut microorganisms in the development and progression of IBD.
Immune Imbalance
Various factors activate the Th1, Th2, and Th17 inflammatory pathways, leading to increased secretion of inflammatory cytokines (e.g., TNF-α, IFN-γ, IL-1β, IL-6, IL-12, IL-23) and an imbalance between pro-inflammatory and anti-inflammatory cytokines. This imbalance results in persistent intestinal mucosal inflammation and damage to the mucosal barrier.
The pathogenesis of IBD can be summarized as follows: environmental factors act on genetically susceptible individuals, and with the involvement of gut microbiota, immune dysregulation occurs, causing damage to the intestinal mucosal barrier and leading to chronic inflammatory injury of the intestinal mucosa.
To be continued