online ISSN 2415-3176
print ISSN 1609-6371
logoExperimental and Clinical Physiology and Biochemistry
  • 12 of 12
Up
ECPB 2019, 87(3): 82–89
https://doi.org/10.25040/ecpb2019.03.082
Research articles

Reproduction of inflammatory bowel diseases in experiment

A.S. TRUSHENKO, V.I. MAMCHUR
Abstract

The incidence of inflammatory bowel diseases, which has recently increased, encourages scientists to search for the most representative and easily reproducible animal models for studying the links of pathogenesis and possible ways of treating of this pathology. This review presents analysis of the genetically-conditioned and chemically-induced models of inflammatory bowel diseases. There are discussed the most common genetically conditioned models based on defects of the immune system links, loss of components of the intestinal epithelium, or spontaneous lesions of the intestinal tube wall. It is also described the techniques of the most appropriate chemically-induced models, as well as the main pathogenetic links in the development of colitis when using chemical agents. In particular, modeling of Crohn's disease with trinitrobenzenesulfonic acid (TBSA), and ulcerative colitis – with dextran sodium sulfate (DSS), as well as other models having common pathogenetic mechanisms of inflammation in the small and large intestine, e.g. models in which acetic acid, peptidoglycan, λ-carrageenan and indomethacin are used as acting chemical agents. Taking into account the correspondence of the reproduction of pathogenetic signs of inflammatory bowel disease in animals to such in people, the complexity of reproduction and the cost of the necessary components, among the discussed techniques, the undeniable advantages belong to the DSS model of ulcerative colitis and TBSA model of the reproduction of Crohn’s disease, and also the indomethacin model of inflammatory processes of the small intestine.

For instance, treatment with DSS causes typical histological characteristics of the disease with such manifestations as erosions, ulcers, infiltration of granulocytes to the lamina propria and submucosal layers of the colon, disposition of crypts with the appearance of a wide gate between the crypt base and the muscular layer, and the occurrence of lymphocytosis. TBSA also causes significant changes in the morphological characteristics, mechanical properties and pharmacological response of the circular muscular layer of the distal intestinal regions. TBSA causes a local increase in the synthesis of proinflammatory mediators, which is associated with a neutrophil response, resulting in profound destructive changes in the distal bowel. Finally, indomethacin, which is a strong non-steroidal anti-inflammatory drug with nonspecific action, causes more damage to the distal jejunum and proximal ileum.

These models allow reproducing the corresponding basic pathogenetic changes in inflammatory bowel disease, which makes it possible to study the systemic and intersystemic cause-effect relationships of pathobiochemical, histological and pathophysiological levels at different stages of the development of the disease and upon pharmacological correction. Our interest in comparative analysis of the existing pathological models, selection of the corresponding adequate modelling schemes for use in our conditions is due to further in-depth study of the pathogenesis of inflammatory bowel disease, as well as further research of pharmacological approaches for correction of these pathological conditions.

Received: 11.07.19

Keywords: Crohn’s disease, ulcerative colitis, trinitrobenzene sulfonic acid; dextran sodium sulfate; indomethacin

Full text: PDF (Ukr) 341K

References
  1. 1. Osikov MV, Simonjan EV, Bakeeva AE, Kostina AA. Experimental modeling of Crohn's disease and ulcerative colitis). Modern problems of science and education. 2016. [in Russian].
  2. 2. Cagatay T, Bingol Z, Kiyan E, Yegin Z, Okumus G, Arseven O et al. Follow-up of 1887 patients receiving tumor necrosis-alpha antagonists: Tuberculin skin test conversion and tuberculosis risk. Clinical Respiratory Journal. 2017. doi.org/10.1111/crj.12726
  3. 3. Yokoyama Y, Kamikozuru K, Watanabe K, Nakamura S. Inflammatory bowel disease patients experiencing a loss of response to infliximab regain long-term response after undergoing granulocyte/monocyte apheresis: A case series. Cytokine. 2017;103:25-8. doi.org/10.1016/j.cyto.2017.12.030
  4. 4. Yamada A, Arakaki R, Saito M, Tsunematsu T, Kudo Y, Ishimaru N. Role of regulatory T cell in the pathogenesis of inflammatory bowel disease. World Journal of Gastroenterology. 2016;22(7):2195-205. doi.org/10.3748/wjg.v22.i7.2195
  5. 5. Eichele DD, Kharbanda KK. Dextran sodium sulfate colitis murine model: An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis. World Journal of Gastroenterology. 2017;23(33):6016-29. doi.org/10.3748/wjg.v23.i33.6016
  6. 6. Randhawa PK, Singh K, Singh N, Jaggi, AS. A review on chemical-induced inflammatory bowel disease models in rodents. The Korean Journal of Physiology & Pharmacology. 2014;18(4):279-88. doi.org/10.4196/kjpp.2014.18.4.279
  7. 7. Araki Y, Bamba T, Mukaisho K, Kanauchi O, Ban H, Bamba S et al. Dextran sulfate sodium administered orally is depolymerized in the stomach and induces cell cycle arrest plus apoptosis in the colon in early mouse colitis. Oncology Reports. 2012;28(5):1597-605. doi.org/10.3892/or.2012.1969
  8. 8. Karaboga I, Demirtas S, Karaca T. Investigation of the relationship between the Th17/ IL-23 pathway and innate-adaptive immune system in TNBS-induced colitis in rats. Iranian Journal of Basic Medical Sciences. 2017;20(8):870-9.
  9. 9. Elson CO, Cong Y, Sundberg J. The C3H/HeJBir mouse model: a high susceptibility phenotype for colitis. International Reviews of Immunology. 2000;19(1):63-75. doi.org/10.3109/08830180009048390
  10. 10. Oertel S, Scholich K, Weigert A, Thomas D, Schmetzer J, Pellizzon CH. et al. Ceramide synthase 2 deficiency aggravates AOM-DSS-induced colitis in mice: role of colon barrier integrity. Cellular and Molecular Life Sciences. 2017;74(16):3039-55. doi.org/10.1007/s00018-017-2518-9
  11. 11. Wunschel EJ, Schirmer B, Seifert R, Neumann D. Lack of Histamine H4-Receptor Expression Aggravates TNBS-Induced Acute Colitis Symptoms in Mice. Frontiers in Pharmacology. 2017;8,642. doi.org/10.3389/fphar.2017.00642
  12. 12. Fitzpatrick LR, Wang J, Le T. Caffeic acid phenethyl ester, an inhibitor of nuclear factor- kappaB, attenuates bacterial peptidoglycan polysaccharide-induced colitis in rats. Journal of Pharmacology and Experimental Therapeutics. 2001;299 (3):915-20.
  13. 13. Reingold L, Rahal K, Schmiedlin-Ren P, Rittershaus AC, Bender D, Owens SR et al. Development of a peptidoglycan-polysaccharide murine model of Crohn's disease: effect of genetic background. Inflammatory bowel disease. 2013;19(6):1238-44. doi.org/10.1097/MIB.0b013e31828132b4
  14. 14. Pricolo VE, Madhere SM, Finkelstein SD, Reichner JS. Effects of lambda-carrageenan induced experimental enterocolitis on splenocyte function and nitric oxide production. Journal of Surgical Research. 1996;66(1):6-11. doi.org/10.1006/jsre.1996.0364
  15. 15. Shin SJ, Noh CK, Lim SG, Lee KM, Lee KJ. Non-steroidal anti-inflammatory drug- induced enteropathy. Intestinal Research. 2017;15(4):446-55. doi.org/10.5217/ir.2017.15.4.446
  16. 16. Tanner SM, Staley EM, Lorenz RG. Altered generation of induced regulatory T cells in the FVB.mdr1a-/- mouse model of colitis. Mucosal Immunology. 2013;6(2):309-23. doi.org/10.1038/mi.2012.73
  17. 17. Ishimaru N, Yamada A, Kohashi M, Arakaki R, Takahashi T, Izumi K, Hayashi Y. Development of inflammatory bowel disease in Long-Evans Cinnamon rats based on CD4+CD25+Foxp3+ regulatory T cell dysfunction. Journal of Immunology. 2008;180(10):6997-7008. doi.org/10.4049/jimmunol.180.10.6997
  18. 18. De Santis S, Kunde D, Galleggiante V, Liso M, Scandiffio L, Serino G et al. TNFα deficiency results in increased IL-1β in an early onset of spontaneous murine colitis. Cell Death and Disease. 2017;8(8),e2993. doi.org/10.1038/cddis.2017.397
  19. 19. Watanabe T, Kitani A, Murray PJ, Wakatsuki Y, Fuss IJ, Strober W. Nucleotide binding oligomerization domain 2 deficiency leads to dysregulated TLR2 signaling and induction of antigen-specific colitis. Immunity. 2006;25(3):473-85. doi.org/10.1016/j.immuni.2006.06.018
  20. 20. Fox JG, Rogers AB, Whary MT, Ge Z, Taylor NS, Xu S et al. Gastroenteritis in NF- kappaB-deficient mice is produced with wild-type Camplyobacter jejuni but not with C. jejuni lacking cytolethal distending toxin despite persistent colonization with both strains. Infection and immunity. 2004;72(2):1116-25. doi.org/10.1128/IAI.72.2.1116-1125.2004
  21. 21. Steinert A, Linas I, Kaya B, Ibrahim M, Schlitzer A, Hruz P et al. The Stimulation of Macrophages with TLR Ligands Supports Increased IL-19 Expression in Inflammatory Bowel Disease Patients and in Colitis Models. The Journal of Immunology. 2017;199(7):2570-84. doi.org/10.4049/jimmunol.1700350
  22. 22. Zhang F, Ma N, Gao YF, Sun LL, Zhang, JG. Therapeutic Effects of 6-Gingerol, 8-Gingerol, and 10-Gingerol on Dextran Sulfate Sodium-Induced Acute Ulcerative Colitis in Rats. Phytotherapy Research. 2017;31(9):1427-32. doi.org/10.1002/ptr.5871
  23. 23. De Morais Lima GR, Machado FD, Perico LL, de Faria FM, Luiz-Ferreira A, Souza Brito AR et al. Anti-inflammatory intestinal activity of Combretum duarteanum Cambess In trinitrobenzenesulfonic acid colitis model. World Journal of Gastroenterology. 2017;23(8):1353-66. doi.org/10.3748/wjg.v23.i8.1353
  24. 24. Chiriac MT, Buchen B, Wandersee A, Hundorfean G, Günther C, Bourjau Y et al. Activation of Epithelial Signal Transducer and Activator of Transcription 1 by Interleukin 28 Controls Mucosal Healing in Mice With Colitis and Is Increased in Mucosa of Patients With Inflammatory Bowel Disease. Gastroenterology. 2017;153(1):123-38.e8. doi.org/10.1053/j.gastro.2017.03.015
  25. 25. Wang X, Ouyang Q, Luo WJ. Oxazolone-induced murine model of ulcerative colitis. Chinese Journal of Digestive Diseases. 2004;5(4):165-8. doi.org/10.1111/j.1443-9573.2004.00173.x
  26. 26. Weigmann B, Neurath MF. Oxazolone-Induced Colitis as a Model of Th2 Immune Responses in the Intestinal Mucosa. Methods in Molecular Biology. 2016;1422:253-61. doi.org/10.1007/978-1-4939-3603-8_23
  27. 27. Zherebiatiev A.S., Kamyshnyi A.M. Influence of simvastatin and interleukin-1 receptor antagonist on the expression of pattern recognition receptors and transcriptional regulation of T-helper cells by colonic lymphocytes during experimental oxazolone-induced colitis in rats). The journal of clinical and experimental morphology. 2015;15(3):42-46. [in Russan].
  28. 28. Hapfelmeier S, Stecher B, Barthel M, Kremer M, Müller AJ, Heikenwalder M et al. The Salmonella pathogenicity island (SPI)-2 and SPI-1 type III secretion systems allow Salmonella serovar typhimurium to trigger colitis via MyD88-dependent and MyD88-independent mechanisms. Journal of Immunology. 2005;174(3):1675-85. doi.org/10.4049/jimmunol.174.3.1675
  29. 29. Davis RB, Kechele DO, Blakeney ES, Pawlak JB, Caron KM. Lymphatic deletion of calcitonin receptor-like receptor exacerbates intestinal inflammation. JCI Insight. 2017;2(6):e92465. doi.org/10.1172/jci.insight.92465
  30. 30. Kawamura T, Kanai T, Dohi T, Uraushihara K, Totsuka T, Iiyama R et al. Ectopic CD40 ligand expression on B cells triggers intestinal inflammation. Journal of Immunology. 2004;172(10):6388-97. doi.org/10.4049/jimmunol.172.10.6388
  31. 31. Cahill RJ, Foltz CJ, Fox JG, Dangler CA, Powrie F, Schauer, DB. Inflammatory bowel disease: an immunity-mediated condition triggered by bacterial infection with Helicobacter hepaticus. Infection and Immunity. 1997;65(8):3126-31.
  32. 32. Spahn TW, Ross M, von Eiff C, Maaser C, Spieker T, Kannengiesser K et al. CD4+ T cells transfer resistance against Citrobacter rodentium-induced infectious colitis by induction of Th 1 immunity. Scandinavian Journal of Immunology. 2008;67(3):238-44. doi.org/10.1111/j.1365-3083.2007.02063.x
  33. 33. Beckwith J, Cong Y, Sundberg JP, Elson CO, Leiter EH. Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigens. Gastroenterology. 2005;129(5):1473-84. doi.org/10.1053/j.gastro.2005.07.057
  34. 34. Chinen T, Kobayashi T, Ogata H, Takaesu G, Takaki H, Hashimoto M et al. Suppressor of cytokine signaling-1 regulates inflammatory bowel disease in which both IFNgamma and IL-4 are involved. Gastroenterology. 2006;130(2):373-88. doi.org/10.1053/j.gastro.2005.10.051
  35. 35. Ishikawa D, Okazawa A, Corridoni D, Jia LG, Wang XM, Guanzon M et al. Tregs are dysfunctional in vivo in a spontaneous murine model of Crohn's disease. Mucosal Immunology. 2013;6(2):267-75. doi.org/10.1038/mi.2012.67


Програмування - Roman.im