Abstract
Ulcerative colitis (UC) is a chronic autoimmune disorder affecting the colonic mucosa. UC is a subtype of inflammatory bowel disease along with Crohn’s disease and presents with varying extraintestinal manifestations. No single etiology for UC has been found, but a combination of genetic and environmental factors is suspected. Research has focused on the role of intestinal dysbiosis in the pathogenesis of UC, including the effects of dysbiosis on the integrity of the colonic mucosal barrier, priming and regulation of the host immune system, chronic inflammation, and progression to tumorigenesis. Characterization of key microbial taxa and their implications in the pathogenesis of UC and colitis-associated cancer (CAC) may present opportunities for modulating intestinal inflammation through microbial-targeted therapies. In this review, we discuss the microbiota-immune crosstalk in UC and CAC, as well as the evolution of microbiota-based therapies.
Highlights
Inflammatory bowel disease (IBD) is a chronic autoimmune condition affecting the gastrointestinal (GI) tract
intestinal epithelial cells (IECs) harvested from patients with active ulcerative colitis (UC) exhibit higher apoptotic indices which contributes to impaired barrier function and permits translocation of commensal and enteropathogenic microorganisms, resulting in higher levels of proinflammatory cytokines including tumor necrosis factor-α (TNF-α) [42]
Antibiotics have been included in UC therapy as adjuvants, both in the presence of active bacterial infection, and for their ability to suppress the abnormal proliferation of pathogens and stabilize the luminal and mucosal microbial load in favor of the growth of beneficial bacteria [116]
Summary
Inflammatory bowel disease (IBD) is a chronic autoimmune condition affecting the gastrointestinal (GI) tract. Exposure to antibiotics during gestation and childhood, psychological stress, and family history affect the risk of developing UC [6] These factors profoundly alter the intestinal microbiome but may provide opportunities for new treatment options. The relationship between UC and CAC has influenced the development of clinical practice guidelines, with increased endoscopic surveillance recommended among UC patients starting 8 years after initial UC diagnosis. These recommendations have led to successful reductions in CAC morbidity and mortality [11]. The mechanisms underpinning UC pathogenesis remain unclear, but the dominant hypothesis suggests that environmental factors, including alterations in intestinal microbiota, contribute to an exaggerated immune response and chronic inflammation in genetically susceptible individuals [12]. This review will discuss key changes in intestinal microbiota associated with UC pathogenesis and immune dysfunction, as well as the role of microbiota-based therapies in affecting intestinal inflammation and progression to neoplasia
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