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.

scholarly journals CCR6–CCL20-Mediated Immunologic Pathways in Inflammatory Bowel Disease

2018 ◽  
Vol 1 (1) ◽  
pp. 15-29 ◽  
Author(s):  
Ranmali Ranasinghe ◽  
Rajaraman Eri
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Systematic Investigation ◽  
Protective Mechanism ◽  
Food Antigens ◽  
Gut Mucosa ◽  
T Helper Lymphocyte ◽  
Inflammatory Bowel ◽  
Underlying Mechanisms

Inflammatory bowel disease (IBD) has evoked significant interest in human immunobiology given its tactical immune evasion methodologies resulting in acute immune destabilization. IBD comprising Crohn’s disease and Ulcerative colitis manifests as chronic inflammation in the gut mucosa, leading to complexities involving immune dysregulation in the T helper lymphocyte arm, effecting disease pathogenicity. The mucosa of the alimentary canal is constantly exposed to a myriad of food antigens and luminal microorganisms for which a consistent host-protective mechanism is operative in healthy people. Lowered mucosal immune expression which allows penetration of the epithelial barrier by infective pathogenic microbes elicits both innate and adaptive immune responses in the gut, culminating in aberrant intestinal inflammation. Interestingly, the IBD leukocyte repertoire is significantly entwined with chemokine-assisted chemotactic navigation into the sites of inflammation, which is also thought to generate favorable immune-suppressive responses. The functions of the cognate chemokine receptor, CCR6, which binds with its unique ligand CCL20, are expected to tilt the balance between upregulation of homeostatic tolerance and inflammatory pathophysiology. This review aims to critically examine the CCR6-driven immune pathways: TH1/TH2, TH1/TH17, TH17/Treg, IL-23/IL-17, Akt/ERK-1/2, ILC3, and TH9/TH2 for systematic investigation of its underlying mechanisms in the future and to underpin its importance in resolving IBD pathology. Thus, CCR6 occupies an exclusive position in gut immunology which renders it an invaluable therapeutic tool for the production of novel medicaments to treat IBD.

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 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 CCR6-CCL20 Signalling Networks in Inflammatory Bowel Disease

2018 ◽  
Author(s):  
Ranmali Ranasinghe ◽  
Rajaraman Eri
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Systematic Investigation ◽  
Protective Mechanism ◽  
Food Antigens ◽  
Gut Mucosa ◽  
T Helper Lymphocyte ◽  
Inflammatory Bowel ◽  
Underlying Mechanisms

Inflammatory bowel disease (IBD) has evoked a significant interest in human immunobiology given its tactical immune evasion methodologies resulting in acute immune destabilization. IBD comprising of Crohn&rsquo;s disease and Ulcerative colitis manifest as chronic inflammation in the gut mucosa, leading to complexities involving immune dysregulation in the T helper lymphocyte arm effecting disease pathogenicity. The mucosa of the alimentary canal is constantly exposed to a myriad of food antigens and luminal microorganisms for which a consistent host-protective mechanism is operative in healthy people. Lowered mucosal immune expression which allows penetration of the epithelial barrier by infective pathogenic microbes, elicits both innate and adaptive immune responses in the gut culminating in aberrant intestinal inflammation. Interestingly, IBD leukocyte repertoire is significantly entwined with chemokine assisted chemotactic navigation into the sites of inflammation which is also thought to generate favourable immune suppressive responses. The functions of the cognate chemokine receptor, CCR6, which binds with its unique ligand CCL20, are expected to tilt the balance between upregulation of homeostatic tolerance and inflammatory pathophysiology. This review aims at critically examining the CCR6 driven immune pathways; TH1/TH2, TH1/TH17, TH17/ Treg, IL-23/IL-17, Akt/ERK-1 /2, ILC3 for systematic investigation of its underlying mechanisms in the future and to underpin its importance in resolving IBD aetiopathology. Thus, CCR6 occupies an exclusive position in gut immunology which renders it an invaluable therapeutic tool for the production of novel medicaments to treat IBD.

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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