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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
Inflammatory cells' role in acetic acid-induced colitis
Mohammad H Sanei1, Fatemeh Hadizadeh2, Peyman Adibi3
1Department of Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Neutrophils may not solely cause oxidative stress in colitis. This finding questions the effectiveness of corticosteroids for treating inflammatory bowel disease (IBD).
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Colitis pathogenesis involves free radicals from inflammatory cells and tissues.
- Corticosteroids can only target inflammatory cells, not tissue-derived factors.
- The role of neutrophils in colitis induction and corticosteroid efficacy requires further investigation.
Purpose of the Study:
- To assess the significance of neutrophils in inducing colitis.
- To evaluate the effectiveness of corticosteroids in treating inflammatory bowel disease (IBD).
Main Methods:
- Thirty-six mice were divided into six groups, with colitis induced by acetic acid enema or ex vivo exposure.
- Control groups received water instead of acetic acid.
- Macroscopic, biochemical (H2O2, FRAP), and pathological analyses were performed on tissue samples.
Main Results:
- Significant differences in neutrophilic infiltration, goblet cell depletion, and H2O2 levels were observed between experimental and control groups.
- Ferric Reducing Ability of Plasma (FRAP) showed significant variations across groups, indicating altered oxidative stress.
- Results suggest neutrophils are not the sole contributors to oxidative processes in colitis.
Conclusions:
- Neutrophils may not be the exclusive cause of oxidative stress in colitis.
- The efficacy of corticosteroids in treating colitis, particularly IBD, is rendered doubtful by these findings.
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