Related Experiment Video
Updated: Aug 7, 2026

Effects of Taste Signaling Protein Abolishment on Gut Inflammation in an Inflammatory Bowel Disease Mouse Model
Published on: November 9, 2018
Intestinal gene expression in TNBS treated mice using genechip and subtractive cDNA analysis: implications for
Shinya Yamamoto1, Kazuto Isuzugawa, Yuji Takahashi
1Laboratory of Animal Breeding, The University of Tokyo, Tokyo 113-8657, Japan.
Abstract:
So far it has proven difficult to identify a causative gene(s) or gene product initiating the events that lead to inflammation of the intestinal mucosa and, ultimately, progression to Crohn's disease (CD), an inflammatory bowel disease. However, gene transcripts identified in the intestine of trinitrobenzene sulfonic acid (TNBS)-treated mice might suggest a clue, and even represent candidate genes leading to inflammation and mucosal damage, and to subsequent fibrosis. In the present study, DNA microarray (13000 transcripts) methodology was applied to mucosal RNA extracted from TNBS-treated mice, some transcripts of which were validated via cDNA subtraction and RT-PCR analyses. Intestinal biopsy samples from CD patients were then analyzed using cDNA mini-array (1300 cDNAs), focusing on gene transcripts associated with cancer and immunity. Mini-array results revealed transcript changes similar and also dissimilar to those found from the DNA microarray analysis. These changes, previously known or newly identified, possibly occurring during the initial and progressive stages of inflammatory conditions may provide a clue to identify marker transcripts and/or targets for the development of future gene therapy.
Insights
Identifying genes involved in Crohn's disease (CD) is challenging. This study used gene expression analysis in mice and CD patients to find potential candidate genes for inflammation and fibrosis, aiding future gene therapy development.
Area of Science:
- Gastroenterology
- Molecular Biology
- Immunology
Background:
- Identifying causative genes for Crohn's disease (CD) and intestinal inflammation remains difficult.
- Gene transcripts in TNBS-treated mice offer potential clues to inflammation, mucosal damage, and fibrosis.
- Understanding early-stage gene expression is crucial for developing effective CD therapies.
Purpose of the Study:
- To identify candidate genes and molecular markers associated with intestinal inflammation and fibrosis.
- To compare gene expression patterns in a mouse model of colitis with those in human Crohn's disease patients.
- To explore potential gene targets for future therapeutic interventions in inflammatory bowel disease.
Main Methods:
- DNA microarray analysis of mucosal RNA from TNBS-treated mice (13,000 transcripts).
- Validation of selected transcripts using cDNA subtraction and RT-PCR.
- cDNA mini-array analysis of intestinal biopsy samples from Crohn's disease patients (1,300 cDNAs), focusing on cancer and immunity genes.
Main Results:
- Microarray analysis identified numerous gene transcripts in TNBS-treated mice.
- cDNA mini-array analysis revealed gene transcript changes in CD patients, some mirroring mouse model findings.
- Both known and novel transcript changes were observed, suggesting roles in initial and progressive inflammatory stages.
Conclusions:
- Gene expression profiling in mouse models and human CD patients can reveal key transcripts.
- Identified transcripts may serve as markers for disease progression or targets for gene therapy.
- Further research into these candidate genes could advance the understanding and treatment of Crohn's disease.

