Insights into IBD Pathogenesis.

Cedars-Sinai Inflammatory Bowel Disease Center, Suite D4063, Los Angeles, CA 90048, USA.
Current Gastroenterology Reports 12/2009; 11(6):473-80. DOI: 10.1007/s11894-009-0072-9
Source: PubMed

ABSTRACT Inflammatory bowel disease (IBD), encompassing Crohn's disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disorder caused by dysregulated immune responses in a genetically predisposed individual. Recent accumulating data, including genome-wide association studies, have identified more than 50 distinct genetic loci that confer susceptibility. We highlight the role of microbial-host interaction, particularly with respect to the overlap of common genetic and pathophysiologic mechanisms of CD and UC, interleukin-22-producing natural killer cells, autophagy, and TL1A, a member of the tumor necrosis factor (TNF) family, in gut homeostasis and IBD pathogenesis. This article focuses on the recent advances in understanding of IBD from the past year, including advances in genetics and immunobiology.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Lymphocyte homing antagonists represent promising therapeutic agents for the treatment of idiopathic inflammatory bowel disease (IBD). Several critical molecules involved in the recruitment of inflammatory cells in the intestine, including integrins and chemokine receptors, have been successfully targeted for the treatment of IBD. These agents have shown great promise for the induction and maintenance of remission for both Crohn disease and ulcerative colitis. This article discusses currently approved prototypic agents for the treatment of IBD (natalizumab, anti-α4 integrin; vedolizumab, anti-α4β7 integrin), and several other agents in the same class currently under development.
    Gastroenterology Clinics of North America 09/2014; 43(3). DOI:10.1016/j.gtc.2014.05.012 · 1.92 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Patients with ulcerative colitis (UC) or Crohn's colitis have a greater risk for developing colorectal cancer (CRC). Many studies have described the evolving epidemiology and risk factors for CRC in patients with inflammatory bowel disease (IBD). Recent evidence indicates that the incidence has been decreasing with the advancement of medical and surgical therapies, and surveillance has emerged as the foundation of prevention. Chemoprophylaxis is another area of research; however, given the limited efficacy of these agents, they are only being used in conjunction with endoscopic surveillance. Our ability to formulate effective strategies for the prevention of this dreaded complication expands as more is discovered of the molecular events underlying IBD carcinogenesis. Management strategies are constantly updated as new evidence and endoscopic techniques emerge. In this paper, we review the literature regarding epidemiology, pathogenesis, risk factors and chemoprophylaxis as well as the latest consensus guidelines for management of dysplasia and neoplasia in IBD patients.
    01/2012; Suppl 8:002. DOI:10.4172/2161-069X.S8-002
  • [Show abstract] [Hide abstract]
    ABSTRACT: A complex mucosal barrier protects as the first line of defense the surface of the healthy intestinal tract from adhesion and invasion by luminal microorganisms. In this review, we provide an overview about the major components of this protective system as for example an intact epithelium, the synthesis of various antimicrobial peptides (AMPs) and the formation of the mucus layer. We highlight the crucial importance of their correct functioning for the maintenance of a proper intestinal function and the prevention of dysbiosis and disease. Barrier disturbances including a defective production of AMPs, alterations in thickness or composition of the intestinal mucus layer, alterations of pattern-recognition receptors, defects in the process of autophagy as well as unresolved endoplasmic reticulum stress result in an inadequate host protection and are thought to play a crucial role in the pathogenesis of the inflammatory bowel diseases Crohn's disease and ulcerative colitis.
    World Journal of Gastroenterology 02/2014; 20(5):1165-1179. DOI:10.3748/wjg.v20.i5.1165 · 2.43 Impact Factor


Available from