Research Articles Supplement 3 · 2014 · pp. 140–143 · Issue page

UPDATE ON INFLAMMATORY BOWEL DISEASES ETHIOPATOGENICS

AL
CO
MI
1 MD. PhD Student, Departament of Gastroenterology and Hepatology, Fundeni Clinical Institute, Bucharest
2 MD. PhD Student, Departament of Gastroenterology and Hepatology, Fundeni Clinical Institute, Bucharest
3 Prof. PhD, Departament of Gastroenterology and Hepatology, Fundeni Clinical Institute, Bucharest
Corresponding author: [email protected]
Accepted 27 March 2026
Available Online 15 December 2014
THE INFLAMMATORY BOWEL DISEASES (IBD) CROHN'S DISEASE (CD) AND ULCERATIVE COLITIS (UC) ARE CHRONIC IMMUNOLOGIC DISEASES THAT CAN LEAD TO DECREASED QUALITY OF LIFE AND INVALIDITY; IBD ARE CHARACTERIZED BY ABERRANT IMMUNE RESPONSES TO INTESTINAL MICROBIOTA IN GENETICALLY SUSCEPTIBLE HOSTS THAT LEAD TO CHRONIC EXCESSIVE INFLAMMATION AND IN TIME TO PROGRESSIVE GUT WALL DESTRUCTION. IBD HAVE AN EUROPEAN INCIDENCE OF 12 TO 25 PER 100,000 PERSON -YEARS, HIGHER FOR UC THAN CD, WITH A PREVALENCE OF 0.5-1%. ENVIRONMENTAL FACTORS LIKE CIGARETTE SMOKING, POLLUTION, CHANGES IN DIET AND EXCESSIVE USE OF ANTIBIOTICS ARE INCRIMINATED IN IBD PATOGENESIS. THERE IS THOUGHT TO EXIST AN IMBALANCE IN THE INNATE AND ACQUIRED IMMUNE RESPONSES TO NORMAL INTESTINAL MICROBIOTA THAT ACTIVATES PRO -INFLAMMATORY CYTOKINES AND LEADS TO A CHRONIC INFLAMMATORY PROCESS AROUND THE GUT BARRIER. THIS IN TIME LEADS TO INTESTINAL BARRIER DESTRUCTION AND EXPOSURE TO EVEN MORE BACTERIAL PARTICLES THAT FURTHER AGGRAVATE THE INFLAMMATORY PROCESS. GENETIC STUDIES HAVE PROVIDED MANY SUSCEPTIBLE LOCI FOR IBD. IT IS KNOWN FROM THE LITERATURE THAT GENETIC FACTORS ACCOUNT FOR 13.6% OF CD AND 7.5% FOR UC VARIANCE. IN THIS LITERATURE REVIEW WE HIGHLIGHT SOME ETHIOPATHOGENIC LEADS THAT ARE RECENT TARGETS OF CLINICAL AND FUNDAMENTAL IBD RESEARCH.
IBD GENETICS IMMUNOLOGY THERAPEUTIC TARGETS
The body of this article is intentionally hidden on the public page. Please use the PDF reader or the PDF download for the complete text.
[1]
Molodecky NA, Soon IS, Rabi DM, et al. Increasing incidence and prevalence o f the inflammatory bowel diseases with time, based on systematic review. Gastroenterology. 2012, 142: 46-54.
[2]
Viladomiu M et al. Nutritional protective mechanisms against gut inflammation. Journal of Nutritional Biochemistry. 2013, 24(6):929-39.
[3]
Aldhous MC, Soo K, Stark LA, et al. Cigarette smoke extract (CSE) delays NOD2 expression and affects NOD2/RIPK2 interactions in intestinal epithelial cells. PloS One. 2011, 6:e24715.
[4]
Cucino C, Sonnenberg A. Occupational mortality from inflammatory bowel disease in th e United States 1991-1996. Am J Gastroenterol. 2001, 96:1101-05.
[5]
Jason K Hou, Bincy Abraham, Hasem El -Serag. Dietary Intake and Risk of Developing Inflammatory Bowel Disease: A Systematic Review of the Literature. Am J Gastroenterol. 2011, 106:563-73.
[6]
Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt (Eds.). Sleisenger and Fordtran's Gastrointestinal and Liver Disease. New York : Sounders Elsevier, 2010. ISBN: 9-7814-1606-1892.
[7]
Gerova VA, Stoynov SG, Katsarov DS, Svinarov DA. Increased intestinal perme ability in inflammatory bowel diseases assessed by iohexol test. World J Gastroenterol. 2011, 17:2211-15.
[8]
Kobayashi T, Okamoto S, Hisamatsu T et al. IL23 differentially regulates the Th1/Th17 balance in ulcerative colitis and Crohn’s disease. Gut. 2008, 57: 1682-89.
[9]
Dige A, Stoy S, Rasmussen TK et al. Increased levels of circulating Th17 cells in quiescent versus active Crohn’s disease. J Crohns Colitis. 2013, 7: 248-55.
[10]
Xu XR, Liu CQ, Feng BS, Liu ZJ. Dysregulation of mucosal immune response in pathogenesi s of inflammatory bowel disease. World J Gastroenterol. 2014, 20(12):3255-64.
[11]
Roediger WE. The colonic epithelium in ulcerative colitis: an energy -deficiency disease? Lancet. 1980, 2: 712-5.
[12]
Fukushima K, Fiocchi C. Paradoxical decrease of mitochondrial DNA deletions in epithelial cells of active ulcerative colitis patients. Am J Physiol Gastrointest Liver Physiol. 2004, 286: G804 13.
[13]
Shkoda A, Ruiz PA, Daniel H, Kim SC, Rogler G, Sartor RB, Haller D. Interleukin-10 blocked endoplasmic reticulum stress in in testinal epithelial cells: impact on chronic inflammation. Gastroenterology. 2007, 132: 190 207.
[14]
Kaser A, Lee AH, Franke A, Glickman JN, Zeissig S, Tilg H, Nieuwenhuis EE, Higgins DE, Schreiber S, Glimcher LH, Blumberg RS. XBP1 links ER stress to intestina l inflammation and confers genetic risk for human inflammatory bowel disease. Cell. 2008, 134: 743-56.
[15]
Hotamisligil GS, Erbay E. Nutrient sensing and inflammation in metabolic diseases. Nat Rev Immunol. 2008, 8: 923-34.
[16]
Beltran B, Nos P, Dasi F et al. Mitochondrial dysfunction, persistent oxidative damage, and catalase inhibition in immune cells of naive and treated Crohn’s disease. Inflamm Bowel Dis. 2010, 16: 76-86.
[17]
Dorn SD, Abad JF, Panagopoulos G, Korelitz BI. Clinical characteristics of familial versus sporadic Crohn’s disease using the Vienna Classification. Inflamm Bowel Dis. 2004, 10:201-6.
[18]
Jostins L, Ripke S, Weersma RK, et al. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature. 2012, 490:119-24.
[19]
Anderson CA, Boucher G, Lees CW, et al. Meta-analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47. Nat Genet. 2011, 43:246-52.
[20]
Brand S. Crohn’s disease: Th1, Th17 or both? The change of a paradi gm: new immunological and genetic insights implicate Th17 cells in the pathogenesis of Crohn’s disease. Gut. 2009, 58:1152-1167.
[21]
Parkes M. Advances in IBD genetics and clinical implications. Journal of Crohn's and Colitis Supplements. 2010, Vol. 4, 1: 3-4.
[22]
Bank S, Andersen PS, Burisch J et al. Associations between functional polymorphisms in the NFκB signaling pathway and response to anti -TNF treatment in Danish patients with inflammatory bowel disease. Pharmacogenomics J. 2014, 14(6):526-34.
[23]
Chassaing B, Darfeuille -Michaud A. The commensal mic robiota and enteropathogens in the pathogenesis of inflammatory bowel diseases. Gastroenterology. 2011, 140: 1720-28.
[24]
Hang Thi Thu Nguyen et al. Crohn's Disease -Associated Adherent Invasive Escherichia coli Modulate Levels of microRNAs in Intestinal Epithelial Cells to Reduce Autophagy. Gastroenterology. 2014, 146: 508-19. Supplement No. 3/2014 INFORMATION ABOUT RESEARCH AND SCIENCE TODAY JOURNAL AIMS AND SCOPE OF THE CONTENT Research and Science Today Journal is a publication founded in 2011 and it is dedicated to the students of all levels (license, master and doctoral), professors and researchers of faculties in the country and abroad. We want to offer the participants the opportunity to present their scientific works in the following areas: Social Sciences, Economic Sc iences, Legal Sciences, Humanities, Education Sciences, Engineering, Medicine and Sport. This journal provides students the opportunity to create and / or to improve their abilities to write scientific papers. So each appearance (two appearances per year at which we can add supplements) contains a number of papers written by students, masters and doctoral from the faculties from the country or / and abroad. The journal promotes original studies contributing to the progress of knowledge and it is motivated by the need to address issues of theory and practice in the areas mentioned above. The Journal is a training means of the factors involved in the conceptualization, development, implementation and evaluation , aiming the formation of creative personalities who could be able to adapt through the changing conditions of life. Journal wants to be a forum for debates disciplinaries and interdisciplinaries theoretical topics, to become a research support, to leverage this work at regional, national and international levels. We believe that this gathering will enjoy the support from both parts of the researchers and of the practitioners, and will provide appropriate training sources held professional through the current problems. Frequency of publication: 2 numb er per year (March and November) and supplement numbers (if it necessary) Peer-review process : All submitted manuscripts are peer -reviewed by members of the Editorial Board. Papers that fit to the topic of the journal are evaluated by two independent scientific reviewers who accepted to review papers and sent to the Editor in Chief the Reviewer Invitation Response Form. Reviewers’ identity is undisclosed to the authors. Reviewers give to the Editor in Chief their Form for Reviewer, with the comments on th e scientific content of the paper and on the opportunity of publishing it. Editor in Chief summarizes reviewers’ observations in order to be communica ted to the corresponding author. Taking into account the opinions of all referees, the Editor in Chief dec ides on the acceptance/revision/rejection of the paper. Upon reviewers' recommendations, the manuscript can be accepted, sent back to author for minor revisions, or rejected. Abstracting and indexing: SSRN, EBSCO, ProQuest, IndexCopernicus, Scipio, Genamics, Ulrich`s Periodicals Directory, DOAJ, MPRA (Ideas, EconPapers, Socionet), HeinOnline, Google Academic, DRJI, CiteFactor. More informations here: http://www.rstjournal.com/indexari-2/ CONTACT: Phone: +40766665670 Mail: [email protected] Web: http://www.rstjournal.com