Differences in epidemiological features between ulcerative colitis and Crohn’s disease: The early life-programmed versus late dysbiosis hypothesis (original) (raw)
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Nutrition Reviews, 2012
Ulcerative colitis and Crohn's disease, collectively known as inflammatory bowel disease, represent the heterogeneous outcome of three colliding influences: genetic risk factors, environmental modifiers, and immune effector mechanisms of tissue injury. The nature of these inputs is complex, with each having distinct and overlapping contributions to ulcerative colitis and Crohn's disease. Identification of specific genetic risk factors has improved the understanding of specific pathways to disease, but the primacy of environmental or lifestyle factors linked to changes in the gut microbiota, particularly in early life, is increasingly evident. Clarification of the molecular basis of host-microbe interactions in health and in susceptible individuals promises novel therapeutic strategies.
Journal of Clinical & Cellular Immunology, 2014
The pathogenesis of inflammatory bowel diseases (IBD), such as ulcerative colitis (UC) and Crohn's disease (CD) is complex, and our knowledge on the topic is constantly growing. The two disorders are distinct, yet overlap in their clinical manifestations and underlying causes. This review aims to provide a broad overview of the numerous pathogenetic factors that can lead to the development of IBD, focusing on novel findings and on the differences between UC and CD. Recent advances in genetics have identified new components in the pathogenesis, as an example, the importance of Th17 lymphocytes and the IL-17/IL-23 pathway have been highlighted in both diseases, apart from the previously known Th1-Th2 driven processes. Genetic background of increased permeability has been explored in UC, and the role of defective autophagy was recently described in CD. Genetic alterations can lead to an exaggerated immune response to the resident microbial flora. This microflora is altered in IBD patients, probably due to their reduced ability to stabilize its bacterial components and due to different environmental factors. An exhaustive exploration of environmental factors is particularly important, as they can be influential in many cases. The impact of smoking is the most established environmental factor, having deleterious effects in CD and protective in UC. Recent opinions on other factors, such as early appendectomy, diet, reduced vitamin D levels, the use of specific medications, breastfeeding, personal hygiene and psychological factors are also discussed. Epigenetics, a new field of research, links environmental factors to genetics. Understanding these factors is of great significance as changing lifestyles and improving life circumstances have started to increase the prevalence of IBD also in developing countries.
Intestinal microbiota: The explosive mixture at the origin of inflammatory bowel disease?
World journal of gastrointestinal pathophysiology, 2014
Inflammatory bowel diseases (IBDs), namely Crohn's disease and ulcerative colitis, are lifelong chronic disorders arising from interactions among genetic, immunological and environmental factors. Although the origin of IBDs is closely linked to immune response alterations, which governs most medical decision-making, recent findings suggest that gut microbiota may be involved in IBD pathogenesis. Epidemiologic evidence and several studies have shown that a dysregulation of gut microbiota (i.e., dysbiosis) may trigger the onset of intestinal disorders such as IBDs. Animal and human investigations focusing on the microbiota-IBD relationship have suggested an altered balance of the intestinal microbial population in the active phase of IBD. Rigorous microbiota typing could, therefore, soon become part of a complete phenotypic analysis of IBD patients. Moreover, individual susceptibility and environmental triggers such as nutrition, medications, age or smoking could modify bacterial ...
Role of gut microbiota in Crohn's disease
Expert Review of Gastroenterology and Hepatology, 2009
Crohn's disease (CD), a form of inflammatory bowel disease (IBD), provides a complex model of host-microbe interactions underpinning disease pathogenesis. Although there is not widespread agreement on the etiology of CD, there is evidence that microorganisms lead to the often severe inflammatory response characteristic of the disease. Despite several microbial candidates, no specific microbe has been considered pathogenic. Instead, the concept of the 'pathogenic community' has emerged from the evidence, whereby the stability of the microbial ecosystem of the healthy human gut is disrupted in response to host genetics and destabilized immunity, perhaps through changing public health practices leading to altered microbial exposures over time. We discuss the complex microbial ecosystem of the mammalian gut, the underlying genetic factors that predispose to CD, and how these gene variants may alter host-microbe interactions and propagate inflammation. Over the next 5 years, the increased understanding of genes involved in CD and the way in which individuals with variants of these genes respond differently to nutrients and drugs will enable the rational development of personalized therapies, using pharmacogenomic and nutrigenomic approaches.
Review Perturbation of the Human Microbiome as a Contributor to Inflammatory Bowel Disease
2014
The human microbiome consist of the composite genome of native flora that have evolved with humanity over millennia and which contains 150-fold more genes than the human genome. A "healthy" microbiome plays an important role in the maintenance of health and prevention of illness, inclusive of autoimmune disease such as inflammatory bowel disease (IBD). IBD is a prevalent spectrum of disorders, most notably defined by Crohn's disease (CD) and ulcerative colitis (UC), which are associated with considerable suffering, morbidity, and cost. This review presents an outline of the loss of a normal microbiome as an etiology of immune dysregulation and IBD pathogenesis initiation. We, furthermore, summarize the knowledge on the role of a healthy microbiome in terms of its diversity and important functional elements and, lastly, conclude with some of the therapeutic interventions and modalities that are now being explored as potential applications of microbiome-host interactions.
Perturbation of the Human Microbiome as a Contributor to Inflammatory Bowel Disease
Pathogens, 2014
The human microbiome consist of the composite genome of native flora that have evolved with humanity over millennia and which contains 150-fold more genes than the human genome. A "healthy" microbiome plays an important role in the maintenance of health and prevention of illness, inclusive of autoimmune disease such as inflammatory bowel disease (IBD). IBD is a prevalent spectrum of disorders, most notably defined by Crohn's disease (CD) and ulcerative colitis (UC), which are associated with considerable suffering, morbidity, and cost. This review presents an outline of the loss of a normal microbiome as an etiology of immune dysregulation and IBD pathogenesis initiation. We, furthermore, summarize the knowledge on the role of a healthy microbiome in terms of its diversity and important functional elements and, lastly, conclude with some of the therapeutic interventions and modalities that are now being explored as potential applications of microbiome-host interactions. OPEN ACCESS Pathogens 2014, 3 511
Therapeutic Advances in Gastroenterology
Inflammatory bowel diseases (IBDs), including ulcerative colitis and Crohn’s disease, are chronic inflammatory disorders of the gastrointestinal tract. With in-depth studies on the mechanisms of the initiation and development of IBD, increasing lines of evidence have focused on the intestinal microbiota in the pathogenesis of IBD. The imbalance between the host and intestinal microbiota induces dysregulated immune response in intestinal mucosa and plays a pivotal role in the initiation of disease and ongoing bowel destruction. This review focuses on recent advances in intestinal microbiota regulation of mucosal immune response as well as novel approaches based on intestinal microbiota alterations in the diagnosis and evaluation of therapeutic response in IBD.
Diet, microbes, and host genetics: the perfect storm in inflammatory bowel diseases
Journal of Gastroenterology, 2013
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Review Article Dysbiosis in the Pathogenesis of Pediatric Inflammatory Bowel Diseases
2015
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Inflammatory bowel diseases (IBDs) are chronic inflammatory conditions of the gastrointestinal tract that occur in genetically susceptible individuals. Crohn’s disease (CD) and ulcerative colitis (UC) are two major types of IBD. In about 20–25 % of patients, disease onset is during childhood and pediatric IBD can be considered the best model for studying immunopathogentic mechanisms. The fundamentals of IBD pathogenesis are considered a defective innate immunity and bacterial killing with overaggressive adaptive immune response. A condition of “dysbiosis”, with alterations of the gutmicrobial composition, is regarded as the basis of IBD pathogenesis. The human gastrointestinal (GI) microbial population is a complex, dynamic ecosystem and consists of up to one thousand different bacterial species. In healthy individuals, intestinal microbiota have a sym...