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Updated: Jul 10, 2026

Basic Three-Dimensional (3D) Intestinal Model System with an Immune Component
Published on: September 1, 2023
FMT from Turkish patients with celiac disease is associated with celiac-like enteropathy features in a rat model
Rugiyya Samadzade1,2, Salih Macin3, Babek Alibayov4
1Department of Medical Microbiology, Faculty of Medicine, Selcuk University, Konya, Turkey. rukiyesamadzade@gmail.com.
Background:
This study investigated whether fecal microbiota transfer (FMT) from Turkish celiac disease (CD) patients is associated with the induction of celiac-like enteropathy features in a rat model.
Methods:
Wistar rats received FMT from 10 CD patients or 10 healthy controls following microbiota depletion. Physiological, histopathological (Marsh-like classification), and inflammatory markers were evaluated.
Results:
The celiac disease fecal microbiota recipient rats (CD-FMT rats)group exhibited weight loss (p < 0.0001) and celiac-like histopathological features in 90% of cases. These included marked villous atrophy and intraepithelial lymphocyte counts > 20 per high-power field (HPF). A weighted kappa analysis (0.667) demonstrated a moderate association between donor Marsh scores and recipient histopathology. Systemic inflammation in the CD-FMT rats group was marked by a two-fold increase in serum IL-17 (~ 245 pg/ml; p < 0.0001) and a three-fold increase in IFN-γ (~ 95 pg/ml; p < 0.001). Additionally, mucosal mRNA expression of IL-15, IL-21, TNF-α, and IFN-α was upregulated approximately three-fold (p < 0.001). Serum β-actin levels were significantly elevated (~ 9.5 ng/ml; p < 0.0001), suggesting increased intestinal injury in this experimental setting.
Conclusion:
FMT from Turkish CD patients was associated with the induction of celiac-like enteropathy features in this rat model. These findings suggest that gut microbiota from celiac disease patients may contribute to celiac-like mucosal and immune alterations in this experimental model, although it is not sufficient alone to induce disease and should be interpreted as a modulatory rather than causal factor.
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