International Journal of Celiac Disease
ISSN (Print): 2334-3427 ISSN (Online): 2334-3486 Website: http://www.sciepub.com/journal/ijcd Editor-in-chief: Samasca Gabriel
Open Access
Journal Browser
Go
International Journal of Celiac Disease. 2016, 4(4), 130-134
DOI: 10.12691/ijcd-4-4-5
Open AccessReview Article

Immune Aspects of the Inflammatory Bowel Disease; Correlations with Celiac Disease

Fabian Caja1, , Pavol Makovicky2 and Luca Vannucci1

1Laboratory of Immunotherapy, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic

2Department of Biology, Pedagogical Faculty, Selye Janos University, Komarno, Slovak Republic

Pub. Date: December 03, 2016

Cite this paper:
Fabian Caja, Pavol Makovicky and Luca Vannucci. Immune Aspects of the Inflammatory Bowel Disease; Correlations with Celiac Disease. International Journal of Celiac Disease. 2016; 4(4):130-134. doi: 10.12691/ijcd-4-4-5

Abstract

Inflammatory bowel diseases (IBD) are serious health problems and are connected with increased risk of colitis-associated colorectal carcinoma (CAC). It is the most common cause of death in the patients with Crohn’s disease and ulcerative colitis. In this short review, we intend to summarise some aspects of the immunological signalling networks that may be involved in the pathogenesis of CAC patients with the perspectives of treatment of the disease. We also focused on the correlation between celiac disease and IBD.

Keywords:
Crohn’s disease ulcerative colitis colorectal cancer celiac disease chronic inflammation cytokine signalling

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

References:

[1]  Molodecky, N.A., et al., Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology, 2012. 142(1): p. 46-54 e42; quiz e30.
 
[2]  Lakatos, L. and P.L. Lakatos, Is the incidence and prevalence of inflammatory bowel diseases increasing in Eastern Europe? Postgrad Med J, 2006. 82(967): p. 332-7.
 
[3]  Burisch, J., et al., East-West gradient in the incidence of inflammatory bowel disease in Europe: the ECCO-EpiCom inception cohort. Gut, 2014. 63(4): p. 588-97.
 
[4]  de Lange, K.M. and J.C. Barrett, Understanding inflammatory bowel disease via immunogenetics. J Autoimmun, 2015. 64: p. 91-100.
 
[5]  Baumgart, D.C. and S.R. Carding, Inflammatory bowel disease: cause and immunobiology. Lancet, 2007. 369(9573): p. 1627-40.
 
[6]  Sands, B.E. and S. Grabert, Epidemiology of inflammatory bowel disease and overview of pathogenesis. Med Health R I, 2009. 92(3): p. 73-7.
 
[7]  Shoda, R., et al., Epidemiologic analysis of Crohn disease in Japan: increased dietary intake of n-6 polyunsaturated fatty acids and animal protein relates to the increased incidence of Crohn disease in Japan. Am J Clin Nutr, 1996. 63(5): p. 741-5.
 
[8]  Agus, A., et al., Western diet induces a shift in microbiota composition enhancing susceptibility to Adherent-Invasive E. coli infection and intestinal inflammation. Sci Rep, 2016. 6: p. 19032.
 
[9]  De Filippo, C., et al., Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa. Proc Natl Acad Sci U S A, 2010. 107(33): p. 14691-6.
 
[10]  Ananthakrishnan, A.N., Epidemiology and risk factors for IBD. Nat Rev Gastroenterol Hepatol, 2015. 12(4): p. 205-17.
 
[11]  Jandaghi, E., et al., Is the Prevalence of Celiac Disease Higher than the General Population in Inflammatory Bowel Diseaese? Middle East J Dig Dis, 2015. 7(2): p. 82-7.
 
[12]  Kocsis, D., et al., Prevalence of inflammatory bowel disease among coeliac disease patients in a Hungarian coeliac centre. BMC Gastroenterol, 2015. 15: p. 141.
 
[13]  Tankova, L., et al., The Association of Crohn’s Disease, Celiac Disease and Selective Ig A Deficiency. International Journal of Celiac Disease, 2016. 4(1): p. 30-33.
 
[14]  Stakheev, D. and L. Vannucci, Celiac Disease: A Short Overview about Immunological Aspects and Role of Microbiota. International Journal of Celiac Disease, 2014. 2(4): p. 144-149.
 
[15]  Castano-Milla, C., M. Chaparro, and J.P. Gisbert, Systematic review with meta-analysis: the declining risk of colorectal cancer in ulcerative colitis. Aliment Pharmacol Ther, 2014. 39(7): p. 645-59.
 
[16]  Ullman, T.A. and S.H. Itzkowitz, Intestinal inflammation and cancer. Gastroenterology, 2011. 140(6): p. 1807-16.
 
[17]  Watanabe, T., et al., Ulcerative colitis-associated colorectal cancer shows a poorer survival than sporadic colorectal cancer: a nationwide Japanese study. Inflamm Bowel Dis, 2011. 17(3): p. 802-8.
 
[18]  Sakurai, T., et al., Stress response protein cirp links inflammation and tumorigenesis in colitis-associated cancer. Cancer Res, 2014. 74(21): p. 6119-28.
 
[19]  Grivennikov, S., et al., IL-6 and Stat3 are required for survival of intestinal epithelial cells and development of colitis-associated cancer. Cancer Cell, 2009. 15(2): p. 103-13.
 
[20]  Serafino, A., et al., WNT-pathway components as predictive markers useful for diagnosis, prevention and therapy in inflammatory bowel disease and sporadic colorectal cancer. Oncotarget, 2014. 5(4): p. 978-92.
 
[21]  Komatsu, M., et al., Tumor necrosis factor-alpha in serum of patients with inflammatory bowel disease as measured by a highly sensitive immuno-PCR. Clin Chem, 2001. 47(7): p. 1297-301.
 
[22]  Bollrath, J., et al., gp130-mediated Stat3 activation in enterocytes regulates cell survival and cell-cycle progression during colitis-associated tumorigenesis. Cancer Cell, 2009. 15(2): p. 91-102.
 
[23]  Li, Y., et al., IL-6-induced DNMT1 activity mediates SOCS3 promoter hypermethylation in ulcerative colitis-related colorectal cancer. Carcinogenesis, 2012. 33(10): p. 1889-96.
 
[24]  Polytarchou, C., et al., MicroRNA214 Is Associated With Progression of Ulcerative Colitis, and Inhibition Reduces Development of Colitis and Colitis-Associated Cancer in Mice. Gastroenterology, 2015. 149(4): p. 981-92 e11.
 
[25]  Kusugami, K., et al., Elevation of interleukin-6 in inflammatory bowel disease is macrophage- and epithelial cell-dependent. Dig Dis Sci, 1995. 40(5): p. 949-59.
 
[26]  Li, Y., et al., Disease-related expression of the IL6/STAT3/SOCS3 signalling pathway in ulcerative colitis and ulcerative colitis-related carcinogenesis. Gut, 2010. 59(2): p. 227-35.
 
[27]  Lin, L., et al., STAT3 is necessary for proliferation and survival in colon cancer-initiating cells. Cancer Res, 2011. 71(23): p. 7226-37.
 
[28]  Mandal, D. and A.D. Levine, Elevated IL-13Ralpha2 in intestinal epithelial cells from ulcerative colitis or colorectal cancer initiates MAPK pathway. Inflamm Bowel Dis, 2010. 16(5): p. 753-64.
 
[29]  Abraham, C. and J. Cho, Interleukin-23/Th17 pathways and inflammatory bowel disease. Inflamm Bowel Dis, 2009. 15(7): p. 1090-100.
 
[30]  Murphy, C.A., et al., Divergent pro- and antiinflammatory roles for IL-23 and IL-12 in joint autoimmune inflammation. J Exp Med, 2003. 198(12): p. 1951-7.
 
[31]  Mangan, P.R., et al., Transforming growth factor-beta induces development of the T(H)17 lineage. Nature, 2006. 441(7090): p. 231-4.
 
[32]  Chae, W.J., et al., Ablation of IL-17A abrogates progression of spontaneous intestinal tumorigenesis. Proc Natl Acad Sci U S A, 2010. 107(12): p. 5540-4.
 
[33]  Hyun, Y.S., et al., Role of IL-17A in the development of colitis-associated cancer. Carcinogenesis, 2012. 33(4): p. 931-6.
 
[34]  Fina, D., et al., Regulation of gut inflammation and th17 cell response by interleukin-21. Gastroenterology, 2008. 134(4): p. 1038-48.
 
[35]  Stolfi, C., et al., Involvement of interleukin-21 in the regulation of colitis-associated colon cancer. J Exp Med, 2011. 208(11): p. 2279-90.
 
[36]  Babyatsky, M.W., G. Rossiter, and D.K. Podolsky, Expression of transforming growth factors alpha and beta in colonic mucosa in inflammatory bowel disease. Gastroenterology, 1996. 110(4): p. 975-84.
 
[37]  Schafer, H., et al., TGF-beta1-dependent L1CAM expression has an essential role in macrophage-induced apoptosis resistance and cell migration of human intestinal epithelial cells. Oncogene, 2013. 32(2): p. 180-9.
 
[38]  Beseda, A., et al., The Malabsorption Syndrome versus Celiac Disease: A Diagnostic Reappraisal. International Journal of Celiac Disease, 2015. 3(4): p. 118-131.
 
[39]  Itzkowitz, S.H., Molecular biology of dysplasia and cancer in inflammatory bowel disease. Gastroenterol Clin North Am, 2006. 35(3): p. 553-71.
 
[40]  Chang, C.L., et al., Oxidative stress inactivates the human DNA mismatch repair system. Am J Physiol Cell Physiol, 2002. 283(1): p. C148-54.
 
[41]  Fleisher, A.S., et al., Microsatellite instability in inflammatory bowel disease-associated neoplastic lesions is associated with hypermethylation and diminished expression of the DNA mismatch repair gene, hMLH1. Cancer Res, 2000. 60(17): p. 4864-8.
 
[42]  Clevers, H. and R. Nusse, Wnt/beta-catenin signaling and disease. Cell, 2012. 149(6): p. 1192-205.
 
[43]  Xing, Y., et al., Expression of Wnt and Notch signaling pathways in inflammatory bowel disease treated with mesenchymal stem cell transplantation: evaluation in a rat model. Stem Cell Res Ther, 2015. 6: p. 101.
 
[44]  Dhir, M., et al., Epigenetic regulation of WNT signaling pathway genes in inflammatory bowel disease (IBD) associated neoplasia. J Gastrointest Surg, 2008. 12(10): p. 1745-53.
 
[45]  Connelly, T.M. and W.A. Koltun, The cancer "fear" in IBD patients: is it still REAL? J Gastrointest Surg, 2014. 18(1): p. 213-8.
 
[46]  Baars, J.E., et al., The risk of inflammatory bowel disease-related colorectal carcinoma is limited: results from a nationwide nested case-control study. Am J Gastroenterol, 2011. 106(2): p. 319-28.
 
[47]  Foersch, S. and M.F. Neurath, Colitis-associated neoplasia: molecular basis and clinical translation. Cell Mol Life Sci, 2014. 71(18): p. 3523-35.
 
[48]  van Schaik, F.D., et al., Thiopurines prevent advanced colorectal neoplasia in patients with inflammatory bowel disease. Gut, 2012. 61(2): p. 235-40.