scholarly journals Considerations for Choosing Appropriate Animal Models to Study Inflammatory Bowel Disease

2016 ◽  
Vol 8 (7) ◽  
pp. 1
Author(s):  
Richard R. E. Uwiera ◽  
Trina C. Uwiera ◽  
Janelle A. Jiminez ◽  
G. Douglas Inglis
Keyword(s):  
Inflammatory Bowel Disease ◽  
Animal Model ◽  
Animal Models ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Disease Process ◽  
Careful Consideration ◽  
Complete Understanding ◽  
Advantages And Disadvantages ◽  
Inflammatory Bowel

<p>This article examines several animal models used to investigate mechanisms involved in the induction and progression of inflammatory bowel disease in people. The use of appropriate animal models to study intestinal inflammation requires careful consideration as each model has strengths and limitations for investigating disease, and no single model provides a complete understanding of the disease process. In as such, it compels researchers to carefully contemplate the advantages and disadvantages of each animal model, and to consider the process of choosing the best animal model(s) as an essential component of the experimental design.</p>

scholarly journals Studies on the Interleukin-10 Gene in Animal Models of Colitis

2001 ◽  
Vol 15 (8) ◽  
pp. 557-558
Author(s):  
Hugh J Freeman
Keyword(s):  
Inflammatory Bowel Disease ◽  
Animal Models ◽  
Bowel Disease ◽  
Inflammatory Process ◽  
Intestinal Inflammation ◽  
Therapeutic Potential ◽  
Interleukin 10 ◽  
Necrosis Factor Alpha ◽  
Inflammatory Bowel ◽  
Deficient Mice

Cytokines play a role in the inflammatory process in colitis and may have therapeutic potential. Interleukin-10 (IL-10) has both immunomodulatory and anti-inflammatory properties. IL-10-deficient mice develop intestinal inflammation with increased tissue levels of other cytokines, including tumour necrosis factor-alpha. In patients with inflammatory bowel disease, impaired IL-10 production by lamina propria T cells occurs and human recombinant IL-10 improves clinical parameters in inflammatory bowel disease (eg, Crohn's disease). There seem to be conflicting results in differing animal models, and the timing of administration of IL-10 relative to onset of colitis may be critical, possibly due to rapid clearance of IL-10. Interestingly, in IL-10 gene-deficient mice raised in germ-free conditions, the intestinal inflammatory changes normally observed in conventional nongerm-free conditions are not detected, suggesting a role for luminal bacteria in the pathogenesis of the inflammatory process.

scholarly journals Role of appendix in the development of inflammatory bowel disease in TCR-alpha mutant mice.

1996 ◽  
Vol 184 (2) ◽  
pp. 707-715 ◽  
Author(s):  
A Mizoguchi ◽  
E Mizoguchi ◽  
C Chiba ◽  
A K Bhan
Keyword(s):  
Inflammatory Bowel Disease ◽  
B Cells ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Embryonic Stem ◽  
Disease Process ◽  
Mutant Mice ◽  
Lymphoid Follicles ◽  
Inflammatory Bowel ◽  
Chronic Intestinal Inflammation

T cell receptor-alpha mutant mice (TCR-alpha-/-), created by gene targeting of the TCR-alpha gene in embryonic stem cells, spontaneously develop inflammatory bowel disease (IBD) resembling human ulcerative colitis. Since gut-associated lymphoid tissue is likely to play an important role in the development of chronic intestinal inflammation, we examined the changes in the appendix lymphoid follicle (ALF) and Peyer's patches (PP) in these mice. We found the structure of the ALF to be remarkably similar to that of the PP in the small intestine; in both instances, lymphoid follicles covered by surface epithelium (dome-formation) were found. The amount of proliferation in the lymphoid follicles of the appendix estimated by in vivo incorporation of 5-bromo-2'deoxyuridine was more than two times that of PP in TCR-alpha-/- mice. ELISPOT assay showed an increase of IgA, IgG1, and IgG2a, but not IgM-secreting B cells in ALF of TCR-alpha-/- mice compared to TCR-alpha+/- control mice. Furthermore, TCR-alpha-/- mice revealed an increase of autoantibody-producing B cells against the cytoskeletal protein tropomyosin in ALF as compared to PP. When TCR-alpha-/- mice underwent appendectomy at a young age (3-5 wk), the number of mesenteric lymph nodes cells at 6-7 mo were markedly less than in the sham-operated TCR-alpha-/- mice. Furthermore, appendectomy at 1 mo of age suppressed the development of IBD, with only 3.3% of these mice developing IBD in the 6-7-mo period of observation. In contrast, approximately 80% of controls, including the sham-operated TCR-alpha-/- mice, developed IBD during this period. These results suggest that ALF, rather than PP, is the priming site of cells involved in the disease process and plays an important role in the development of IBD in TCR-alpha-/- mice.

scholarly journals A Novel Urease-Negative HelicobacterSpecies Associated with Colitis and Typhlitis in IL-10-Deficient Mice

1999 ◽  
Vol 67 (4) ◽  
pp. 1757-1762 ◽  
Author(s):  
James G. Fox ◽  
Peter L. Gorelick ◽  
Marika C. Kullberg ◽  
Zhongming Ge ◽  
Floyd E. Dewhirst ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Complex Disease ◽  
Intestinal Inflammation ◽  
Disease Process ◽  
Interleukin 10 ◽  
Rrna Gene ◽  
The Novel ◽  
Inflammatory Bowel ◽  
Immunocompetent Mice

ABSTRACT A spiral-shaped bacterium with bipolar, single-sheathed flagella was isolated from the intestines of IL-10 (interleukin-10)-deficient (IL-10−/−) mice with inflammatory bowel disease. The organism was microaerobic, grew at 37 and 42°C, and was oxidase and catalase positive but urease negative. On the basis of 16S rRNA gene sequence analysis and biochemical and phenotypic criteria, the organism is classified as a novel helicobacter. Cesarean section-rederived IL-10−/− mice without helicobacter infection did not have histological evidence of intestinal inflammation. However, helicobacter-free IL-10−/−, SCID/NCr, and A/JNCr mice experimentally inoculated with the novel urease-negativeHelicobacter sp. developed variable degrees of inflammation in the lower intestine, and in immunocompetent mice, the experimental infection was accompanied by a corresponding elevated immunoglobulin G antibody response to the novel Helicobacter sp. antigen. These data support other recent studies which demonstrate that multipleHelicobacter spp. in both naturally and experimentally infected mice can induce inflammatory bowel disease. The mouse model of helicobacter-associated intestinal inflammation should prove valuable in understanding how specific microbial antigens influence a complex disease process.

scholarly journals An Update of Research Animal Models of Inflammatory Bowel Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Zineb Baydi ◽  
Youness Limami ◽  
Loubna Khalki ◽  
Nabil Zaid ◽  
Abdallah Naya ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Animal Models ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Therapeutic Strategies ◽  
Murine Models ◽  
Immune System Dysfunction ◽  
Inflammatory Bowel ◽  
Underlying Mechanisms ◽  
And Shifts

Inflammatory bowel disease (IBD) is a group of chronic disorders that includes two main disease forms, Crohn’s disease, and ulcerative colitis. The understanding of the intestinal inflammation occurring in IBD has been immeasurably advanced by the development of the now numerous murine models of intestinal inflammation. The usefulness of this research tool in IBD arises from a convergence of underlying genetic susceptibility, immune system dysfunction, environmental factors, and shifts in gut microbiota. Due to the multifactorial feature of these diseases, different animal models have been used to investigate the underlying mechanisms and develop potential therapeutic strategies. The results of preclinical efficacy studies often inform the progression of therapeutic strategies. This review describes the distinct feature and limitations of each murine IBD model and discusses the previous and current lessons from the IBD models.

Activation of A2A Adenosine Receptor Attenuates Intestinal Inflammation in Animal Models of Inflammatory Bowel Disease

2005 ◽  
Vol 129 (1) ◽  
pp. 26-33 ◽  
Author(s):  
Masaru Odashima ◽  
Giorgos Bamias ◽  
Jesus Rivera-Nieves ◽  
Joel Linden ◽  
Cynthia C. Nast ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Animal Models ◽  
Adenosine Receptor ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
A2a Adenosine Receptor ◽  
Inflammatory Bowel

scholarly journals Reducing Pain in Experimental Models of Intestinal Inflammation Affects the Immune Response

2021 ◽  
Author(s):  
Laura Golusda ◽  
Anja A Kühl ◽  
Britta Siegmund ◽  
Daniela Paclik
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune Response ◽  
Animal Models ◽  
Bowel Disease ◽  
Inflammatory Process ◽  
Intestinal Inflammation ◽  
Pain Medication ◽  
Experimental Models ◽  
Current Form ◽  
Inflammatory Bowel

Abstract The incidence of inflammatory bowel disease with its two main manifestations, colitis ulcerosa and Crohn’s disease, is rising globally year after year. There is still a tremendous need to study the underlying pathomechanisms and a well-established tool in order to better understand the disease are colitis models in rodents. Since the concept of the 3Rs was proposed by Russell and Burch, this would include pain medication in animal models of intestinal inflammation as a reduction of suffering. This review argues against pain medication because the administration of pain medication in its current form has an impact on the inflammatory process and the immune response, thus falsifying the results and the reproducibility and therefore leading to misconceptions.

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