Increase In Incidence Of Inflammatory Bowel Disease Research Articles

Insights Into Inflammatory Bowel Disease and Effects of Dietary Fatty Acid Intake With a Focus on Polyunsaturated Fatty Acids Using Preclinical Models.

While the aetiology of inflammatory bowel disease (IBD) has been linked to genetic susceptibility coupled with environmental factors, the underlying molecular mechanisms remain unclear. Among the environmental factors, diet and the gut microbiota have been implicated as drivers of immune dysregulation in IBD. Indeed, epidemiologic studies have highlighted that the increase in incidence of IBD parallels the increase in dietary intake of omega-6 (n-6) polyunsaturated fatty acids (PUFAs) and the change in balance of intake of n-6 to n-3 fatty acids. Experimental evidence suggests that the increase in n-6 PUFA intake increases cell membrane arachidonic acid, which is accompanied by the production of pro-inflammatory mediators as well as increased oxidative stress; together, this contributes to the development of chronic inflammation. However, it is also increasingly clear that some of the n-6 PUFA-derived mediators exert beneficial effects depending on the settings and timing of ingestion. In contrast to n-6, when n-3 PUFA eicosapentaenoic acid and docosahexaenoic acid are incorporated into the cell membrane and are metabolized into less pro-inflammatory eicosanoids, as well as strong specialized pro-resolving mediators, which play a role in inflammation cessation. With a focus on preclinical models, we explore the relationship between dietary lipid, the gut microbiome, and intestinal inflammation.

East Meets West: The Increasing Incidence of Inflammatory Bowel Disease in Asia as a Paradigm for Environmental Effects on the Pathogenesis of Immune-Mediated Disease

East Meets West: The Increasing Incidence of Inflammatory Bowel Disease in Asia as a Paradigm for Environmental Effects on the Pathogenesis of Immune-Mediated Disease

Epidemiologic Clues to Inflammatory Bowel Disease

In this article, the recent literature exploring the epidemiology of inflammatory bowel disease (IBD) is reviewed. Epidemiologic studies present data on disease burden, but may also provide clues to disease etiology. The emergence of IBD in developing nations warrants a systematic search for environmental changes in those countries to explain the evolution of IBD. The hygiene hypothesis suggests that an alteration in the microbial environment experienced by the host facilitates the evolution of chronic immune-mediated diseases. One complex database study suggested that areas with high species richness of human intestinal helminthes are areas with genetic changes in interleukin gene loci. In other words, over the years, the microbial ecology has affected human genetics, which in turn would have an impact on immune responses. Other factors affect the gut microbiome, and several studies have explored the increase in incidence of IBD in relation to such factors as exogenous infections, use of antibiotics, and diet.

Review: Current trends in inflammatory bowel disease: the natural history

The description of the prognosis of inflammatory bowel disease (IBD) is based on systematic follow-up of population-based cohorts. A steady increase in incidence of IBD has occurred. The distribution of ulcerative colitis (UC) is fairly uniform with a preponderance of left-sided disease. One-third of Crohn's disease (CD) patients present with colonic disease, one-third with ileocolonic disease and one-third with small bowel disease. IBD is associated with extra-intestinal manifestations (EIMs) in up to 36% of patients. Uveitis and episcleritis are the most common. The cumulative probability of a relapsing course in UC is 90% after 25 years. In CD disease behaviour varies substantially with time. At diagnosis behaviour is inflammatory in 70% of patients. At follow-up there is a change to either stricturing or penetrating disease. Most patients with CD will eventually require surgery. Risk factors for CD recurrence after surgery include penetrating/fistulizing disease behaviour, young age, short duration of disease before first surgery and ileocolonic disease. The incidence of colorectal cancer (CRC) in UC seems to be decreasing. The risk of CRC in CD seems to be equivalent to the risk in UC. Patients with small bowel CD are also at increased risk of small bowel adenocarcinoma. CD is associated with a mortality rate 20-70% higher than expected, whereas mortality in UC is equivalent to that of the general population. The improved prognosis of IBD, especially UC, could be due to a chemopreventive effect of the medications used. Further studies are needed to develop the best strategy for the reduction of mortality and cancer risk in IBD.

Animal Models of Inflammatory Bowel Disease at the Dawn of the New Genetics Era

Crohn disease (CD) and ulcerative colitis (UC) are chronic inflammatory intestinal diseases with multifactorial etiologies. CD and UC are distinguished both by the location and by the nature of the inflammation. CD displays a transmural discontinuous inflammation, often with granulomas, in any part of the digestive system (most often ileum and/or colon). UC is almost exclusively restricted to the colon with a continuous superficial mucosal and submucosal inflammation. Both CD and UC can be further subphenotyped, suggesting that there is heterogeneity within each disorder. Despite many clinical and pathological features that distinguish CD and UC, the collective term inflammatory bowel disease (IBD) is often used for the two diseases. Clustering of IBD in families without specificity for a given form of IBD supports the notion of common genetic factors in the etiologies of the two conditions. In addition, higher concordance rates in monozygotic twins than dizygotic twins, particularly in CD, points to the importance of genes [1]. Recent advances in genetics have proven that both CD and UC are truly polygenic, but there are also strong environmental influences on IBD. This notion is first and foremost supported by the rapid increase in incidence of IBD during the past 50 years. Understanding the complex interplay between genetic and environmental factors that lead to IBD is a formidable challenge. Animal models have been very helpful in this respect, providing fundamental insight into the importance of immunologic dysregulation and intestinal microbiota [2,3]. Animal models are continuing to give new insights into the pathogenesis of IBD, as shown by two recent papers in PLoS Medicine [4,5]. Simultaneously, there have been remarkable advances in the understanding of the genetics of human IBD, and the mapping of IBD genes is continuously progressing [6–8]. The new genetic findings bear promise for new and better therapies. This translation of basic science into the clinic will be much facilitated by relevant and good animal models. We can thus expect that the new genetic findings will set the stage for future development of animal models in IBD.