An Update of Research Animal Models of Inflammatory Bowel Disease.

Zineb Baydi,Youness Limami,Abdallah Naya,El Mostafa Mtairag,Loubna Khalki,Mounia Oudghiri,Younes Zaid,Nabil Zaid,Toshimi Chiba

doi:10.1155/2021/7479540

Abstract

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.

Highlights

Inflammatory bowel disease (IBD) is a multifactorial or even multigenic disease, affecting roughly 1 million to 1.5 million patients in the United States [1,2,3]. e population of North Africa and Europe are the most affected by IBD; the epidemiology of this disease increased considerably in the mid-twentieth century [4].In 1957, Dr Kirsner and colleagues first invented an experimental colitis model, which was induced in rabbits by sensitization to crystalline egg albumin together with small rectal instillation of dilute formalin [5]. ey tested this model by sensitizing rabbits to crystalline egg albumin by a rectal instillation technique of dilute formalin
A significant progress in the development of mouse models of intestinal inflammation shows that the adoptive transfer of naive CD4+ T-cells (CD4+CD45RBhigh T-cells) from donor mice to SCID or RAG1 mice/syngeneic immunodeficient SCID or RAG1 mice/recipients induces an aggravation of the disease and a colonic inflammation, which develops 5 to 10 weeks after the treatment
We start from the assumption that T-lymphocytes have function differences, which express the various CD45 isoforms; we studied the expression of CD45RA, CD45RO, and CD45RB by peripheral and intestinal T-lymphocytes of IBD patients and compared them to healthy patients

Summary

Introduction

Inflammatory bowel disease (IBD) is a multifactorial or even multigenic disease, affecting roughly 1 million to 1.5 million patients in the United States [1,2,3]. e population of North Africa and Europe are the most affected by IBD; the epidemiology of this disease increased considerably in the mid-twentieth century [4]. In 1957, Dr Kirsner and colleagues first invented an experimental colitis model, which was induced in rabbits by sensitization to crystalline egg albumin together with small rectal instillation of dilute formalin [5]. They have identified genetically modified rats carrying the human HLA-B27 gene to develop colitis [9]. There have since been well over 40 different kinds of genetically engineered KO mouse strains and congenital gene mutant mouse strains found to develop colitis and/or ileitis spontaneously. Modified mice clearly suggest the spontaneous development of colitis/ileitis in many alternative styles of strains whose IBD is mediated by extremely complicated mechanisms [12]. It is approved that genetically modified mice lacking sensitivity (KO) or overexpressing (transgenic (Tg)) to IBD or candidate genes spontaneously develop intestinal inflammation. Ey include IL-10 KO, STAT3 KO, XBP1 KO, IL-2Ra KO, TNFSF15 Tg, and IL-7 Tg mice. is review summarizes the IBD mouse models currently available, in addition to the limitations for each model

Chemically Induced Experimental Models

Adoptive T-Cell Transfer Experimental Model

Genetically Engineered Experimental Model

Spontaneous Mutation Mouse Models

Microbiome-Induced Mouse Models

Conclusion