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Printable Handouts
Navigable Slide Index
- Introduction
- Overview
- Crohn's Disease (CD) and Ulcerative Colitis (UC)
- Mucosal Immunology
- Context of IBD
- Mouse models of intestinal inflammation
- Spontaneous colitis (1)
- Spontaneous colitis (2)
- Colitis caused by genetic manipulation (1)
- Colitis caused by genetic manipulation (2)
- IL-10 KO mice
- IL-10 KO mice get colitis, anti-TNF therapy works
- Colitis induced by exogenous agents
- TNBS colitis model
- Comparison of animal hapten-models of colitis
- Body weight parameters
- Different strains, different methods
- Use of TNBS models
- Acute DSS colitis
- Chronic DSS colitis
- No DSS colitis after antibiotic treatment
- Parameters of disease in chemically induced colitis
- Histology score (DSS and TNBS)
- Disease activity index (DAI)
- Endoscopic evaluation of mice
- Colitis due to manipulation of the immune system
- CD45RB-high transfer model
- CD4+CD45RB-high cells induce a wasting disease
- Histological characteristics
- Giant granuloma cells as diagnosis of CD
- Parameters and important points in the model
- Transfer model protocol & histolgical score system
- CD45RB-high model
- Animal models of mucosal inflammation
- What did we learn from IBD animal models
- Different genetic abnormalities can result in colitis
- STAT-4 transgenic mice develop chronic colitis
- Role of GWAS susceptibility genes
- Susceptibility & genetic background
- Microbiota & the development of colitis
- The gut microbiota
- Colitis in models of mucosal inflammation
- Microbiota differs between suppliers
- Impact on animal studies acknowledged
- Essential role for antigen presenting cells
- Sampling by DCs of antigens in the intestinal lumen
- Essential role for excessive effector T cell function
- Essential role for deficient regulatory T cell function
- Essential role for macrophages
- Essential role of the mucosal barrier
- Muc2-deficient mice develop colitis
- What did we learn from IBD animal models
- What did we learn from IBD pathogenesis
- Which model to choose
- Choosing a model that is comparable to human IBD
- Comparing Models
- Claims from intervention studies
- Actual usage of IBD models
- Acknowledgements
Topics Covered
- Inflammatory bowel diseases (IBD)
- Spontaneous colitis
- Colitis due to targeted mutations or transgenes
- Colitis induced by exogenous agents
- Colitis due to manipulation of the immune system
- Conclusions drawn from IBD animal models
- Choosing an appropriate animal model
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
te Velde, A. (2015, July 30). Animal models of inflammatory bowel disease [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 21, 2024, from https://doi.org/10.69645/XJEX9095.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. Anje te Velde has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Other Talks in the Series: Animal Models in Biomedical Research
Transcript
Please wait while the transcript is being prepared...
0:00
ANJE A. TE VELDE, PHD: Hello.
My name is Anje te Velde.
I am a TI at the
Tytgat Institute for
Liver and Intestinal
Research in Amsterdam.
0:08
During this talk I
will introduce you
to the inflammatory bowel diseases.
In short, IBD.
Then I will give an
overview of the different
experimental colitis models
that are currently used.
The field of IBD research
has had great benefits
from these experimental
colitis models
in the understanding of the
pathogenesis of the disease.
We have learned a great
deal from these models
about the involvement of
genetics, the microbiota,
and the role of different cells
in the development of the disease.
Finally, I will give some
guidance to the decision-making
of which model to choose
for your experiments.
0:46
IBD covers two types of chronic
intestinal inflammation:
Crohn's disease and
Ulcerative Colitis.
Patients suffer from chronic
relapsing intestinal inflammation
leading to abdominal pain, bloody
diarrhea, weight loss, and fatigue.
Most patients are diagnosed
between their second
and fourth decade of life.
Patients need chronic
medical treatments.
However, refractoriness and loss
of response are major problems.
Characteristically, Crohn's disease can
affect entire gastrointestinal tracts,
resulting in discontinuous
transmural ulcers,
mainly in the terminal ilium
and right-sided large intestine.
Ulcerative colitis
continuously affects
the mucosa of the large intestine.
1:34
In the mucosa, there's the tight
regulation of the immune response,
characterized in
the normal situation
by a balance between a sufficient
response to potential pathogens,
and no response to
nonpathogenic commensal bacteria
and compounds of the diet.