| International Session (Symposium) 1 (JSGE・JGES) |
| Thu. November 1st 9:00 - 12:00 Room 13: Kobe International Conference Center International Conference Room |
| Understanding Epidemiology and Microbiome in IBD | |||
| Siew Chien Ng | |||
| Department of Medicine and Therapeutics, The Chinese University of Hong Kong | |||
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| IBD is a global disease in the 21st century. The highest reported prevalence per 100,000 were in Europe and North America. Prevalence exceeds 0.3% in North America, Oceania, and many countries in Europe. Overall, 70.0% of CD and 83.3% of UC studies demonstrated stable or decreasing incidence of IBD in North America and Europe. Since 1990, incidence has been rising in newly industrialized countries outside the Western world, including Brazil and Taiwan. At the turn of the 21st century, IBD has become a global disease with accelerating incidence in newly industrialized countries whose societies have become more Westernized. While incidence is stabilizing or reducing in the Western world, the burden remains high as prevalence surpasses 0.3%. These data highlight the urgent need for research into interventions to prevent IBD and innovations in healthcare systems to manage this complex and costly disease Host genetics and intestinal microbes can both contribute to an individual’s overall susceptibility to IBD. Over 200 genetic variants have been associated with risk for IBD via affecting barrier function or autophagic clearance of intracellular bacteria. Most of the evidence relating to possible causal genes points to an essential role for host defence against infection in IBD. Moreover, 70% of the genetic loci that are associated with IBD are also shared by a variety of autoimmune diseases suggesting that a variety of complex autoimmune diseases share common environmental influences with IBD. The changing epidemiology of inflammatory bowel disease (IBD) across time and geography suggests that environmental factors play a major role in modifying disease expression.. Ulcerative colitis (UC) has emerged first followed by Crohn's disease (CD) after a variable period of time. Improved physician awareness and diagnostic methods are unlikely to fully account for this rapid increase. This epidemiological shift likely relates to increased contact with the West, changes in diet, increasing antibiotics use, improved hygiene, vaccinations, or changes in the gut microbiota, as part of the socioeconomic development in Asia. It has been shown that interactions between genetic (ATG16L1/NOD2) and microbial factors cooperate to promote beneficial immune responses. Secondly, an interaction between a specific virus infection and a mutation in the Crohn’s disease susceptibility gene Atg16L1 induces intestinal pathologies in mice. Disease localisation or complication may also be a major determinant of the IBD-associated gut microbiota composition. Traditional antibiotics, probiotics, and prebiotics appeared to have limited efficacy. Hence, the host:microbe interface holds an important role in transformative medicine for IBD which involved targeting the microbiome via targeted immune modulation, organism-directed antibiotics, and host:microbial population modulators. A better understanding of gene-microbiota interactions that precede the onset of IBD and their interaction with host genetics can lead to new IBD therapeutics and the potential of microbial prevention strategies as well as microbial markers that can predict patient outcome. In the 21st century, urbanization represents a major demographic shift both in the developed and developing worlds. The rapid urbanization experienced in the developing world has been associated with increasing incidence of many forms of autoimmune diseases including IBD. We discussed how urbanization and its surrogates have impacted on the microbiome in both health and inflammatory bowel disease (IBD). The changing epidemiology of IBD globally with increasing disease incidence across many countries relates to westernization of lifestyle and industrialization. The rising incidence of IBD during the process of urbanization within the same genetic background provides evidence of the effect of environment in IBD pathogenesis. The altered environmental factors implicated to be linked to IBD during urbanization, such as changed diet, antibiotic use, pollution, improved hygiene status and early life microbial exposures, have been identified to play a role in changes in the gut microbiota ecology. The synchronous distinction in IBD prevalence and microbiome configuration between rural and urban areas offer us a window to entangle the contribution of rural microbiomes to protect humans against IBD. We will discuss the effect of urbanization and its surrogates on gut microbiome, a broad term herein encompassing bacterial microbiome, virome, fungi and helminths, and how these discrepancies impact on IBD development. |
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