The Genetics of Inflammatory Bowel Disease

Inflammatory Bowel Disease Center, Section of Digestive Diseases, Yale University, New Haven, Connecticut 06520-8019, USA.
Gastroenterology (Impact Factor: 16.72). 11/2007; 133(4):1327-39. DOI: 10.1053/j.gastro.2007.08.032
Source: PubMed
3 Reads
  • Source
    • "A positive family history remains the most important independent risk factor for developing CD to date [4] [13]. More recently, genome-wide analysis studies have revealed more than 30 loci associated with CD [1] [14] [15]. Of significance may be the genetic polymorphisms that alter adaptive immunity and the mutations associated with inadequate surveillance of bacteria by the intestinal mucosa [16] [17] [18] [19] [20]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Crohn's disease (CD) is an inflammatory disorder of the gastrointestinal tract that is likely caused by an inappropriate mucosal inflammatory response to intestinal bacteria in a genetically predisposed host. The lesions of CD can involve any region of the GI tract as well as extraintestinal sites such as the skin, joints, and eyes. The most common presenting symptoms are abdominal pain and prolonged diarrhea associated with fevers, fatigue, and malaise. Delayed growth and failure to thrive may also be observed in pediatric patients. Oral manifestations of CD are known as oral CD and may precede GI involvement, thus serving as early markers of this condition. We describe a 6-year-old male who presented with oral lesions as his initial manifestation of disease and review the current literature pertaining to oral CD.
    Full-text · Article · Aug 2015
  • Source
    • "gliadin), saturated fatty acids, food additives, toothpaste (aluminosilicicates), pathogen associated molecular patterns (PAMPs), or infections change intestinal permeability and microbioma by disrupting apical junctional complexes or damage the protective mucosal layer [1] [20]. These mechanisms lead to an increased exposure of bacterial products, with an increased immune stimulation and activation of adaptive immunity, which in turn leads to a loss of tolerance to autologous enteric flora, for aberrant immune response and inflammation as observed in rats [21][23]. Moreover as reported by Kao et al. [24] in according to the hygiene hypothesis of Gearry RB [4], exposure to fewer microbes and less microbial communities at early age may lead to development of immune system less able to " tolerate " exposure to microbial laden environment later in life leading to inappropriate immune activation . "

    Full-text · Article · Jan 2015 · Open Journal of Gastroenterology
  • Source
    • "Although the nature and anatomical location of the inflammatory pathology differ between the two disorders, it is thought that both arise as a result of an abnormal immune response to the intestinal microbiota in genetically predisposed individuals. In Crohn's disease inflammation is transmural, can be granulomatous, and occurs in any part of the gastrointestinal tract although the ileum is mainly affected, whereas in ulcerative colitis, the pathology impacts primarily the colonic mucosa (Podolsky, 2002). Since the 1940s, the incidence of IBD has dramatically increased in countries with a more ''westernized'' lifestyle, suggesting the influence of environmental factors, including lifestyle, hygiene, diet, and use of antibiotics, all of which may alter the microbiota in favor of disease onset and/or progression (Shanahan and Bernstein, 2009). "

    Full-text · Dataset · Jan 2014
Show more