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Updated: Sep 29, 2025

Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
NF-kB pathway is involved in microscopic colitis pathogenesis
Laura Francesca Pisani1, Gianeugenio Tontini2,3, Maurizio Vecchi2,3
1Gastroenterology and Endoscopy Unit, IRCCS Policlinico San Donato, San Donato Milanese, Italy.
Objective:
To investigate the potential inflammatory pathways involved in the development of microscopic colitis (MC).
Methods:
This prospective study analysed human intestinal tissue that was collected and classified as healthy controls (HC), microscopic colitis (MC) and ulcerative colitis (UC). An RT2 Profiler PCR Array for human inflammatory response and autoimmunity was used to evaluate the expression of 84 specific genes related to the inflammatory and autoimmunity pathways. Data were validated by means of real-time polymerase chain reaction on an independent group of MC intestinal tissue samples.
Results:
This study measured the expression of inflammatory genes in HC (n = 10), in patients with MC (n = 8) and in patients with active UC (n = 10). Of the 84 genes included in the array, the expression of the C-C motif chemokine ligand 19, C-C motif chemokine ligand 21, lymphotoxin beta and complement C3 genes that are involved in the non-canonical nuclear transcription factor kappa B (NF-kB) pathway was increased by 2.96, 6.05, 5.96 and 5.93 times in MC compared with HC, respectively. These results were confirmed by real-time polymerase chain reaction.
Conclusions:
The findings suggest that an impairment of the non-canonical NF-kB pathway is involved in the development of MC.
Insights
Microscopic colitis (MC) development involves impaired non-canonical nuclear transcription factor kappa B (NF-kB) inflammatory pathways. This study identified increased expression of specific NF-kB pathway genes in MC patients compared to healthy controls.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Microscopic colitis (MC) is an inflammatory bowel disease.
- The precise inflammatory pathways driving MC pathogenesis remain incompletely understood.
Purpose of the Study:
- To investigate the inflammatory pathways implicated in the development of microscopic colitis (MC).
Main Methods:
- Prospective analysis of human intestinal tissues from healthy controls (HC), MC patients, and ulcerative colitis (UC) patients.
- Utilized RT2 Profiler PCR Array to assess 84 inflammatory and autoimmunity genes.
- Validated findings using real-time polymerase chain reaction (PCR) on independent MC samples.
Main Results:
- Gene expression analysis revealed significantly increased levels of C-C motif chemokine ligand 19, C-C motif chemokine ligand 21, lymphotoxin beta, and complement C3 in MC patients compared to HC.
- These upregulated genes are integral components of the non-canonical nuclear transcription factor kappa B (NF-kB) pathway.
- Real-time PCR confirmed these elevated gene expression patterns in MC.
Conclusions:
- The study findings indicate a potential impairment in the non-canonical NF-kB pathway contributes to the development of microscopic colitis.
- This suggests the non-canonical NF-kB pathway as a potential therapeutic target for MC.
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