Intestinal Fibrosis
Intestinal Fibrosis - Related Videos
07:04
Forskolin-induced Swelling in Intestinal Organoids: An In Vitro Assay for Assessing Drug Response in Cystic Fibrosis Patients
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Cited by 121 •
2017
This protocol describes an assay for measuring CFTR function and CFTR modulator responses in cultured tissue from subjects with cystic fibrosis (CF). Biopsy-derived intestinal organoids swell in a cAMP-driven fashion, a response that is defective (or strongly reduced) in CF organoids and can be restored by exposure to CFTR modulators.
08:40
Chronic Salmonella Infection Induced Intestinal Fibrosis
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Cited by 4 •
2019
This protocol describes a mouse model of Salmonella driven intestinal fibrosis that resembles key pathological hallmarks of Crohn’s disease including transmural inflammation and fibrosis. This method can be used to evaluate host factors that alter fibrotic outcomes using mutant mice maintained on a C57Bl/6 genetic background.
09:44
Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis
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2025
This protocol demonstrates how the Src homology 2 domain-containing 5'-inositol phosphatase (SHIP)-deficient mouse model of Crohn disease (CD)-like ileal inflammation and fibrosis can be used to test novel therapeutics for CD.
10:58
A Protocol for Lentiviral Transduction and Downstream Analysis of Intestinal Organoids
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Cited by 81 •
2015
In this video protocol we give a step by step explanation of lentiviral transduction in organoids of primary intestinal epithelium and of processing and downstream analysis of these cultures by quantitative RT-PCR, RNA-microarray and immunohistochemistry.
04:37
Intestinal Crypts Isolation: A Method to Isolate Whole Crypts from Small Intestine of Murine Model
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2023
In this video, we demonstrate a technique to isolate whole crypts from a mouse’s small intestine. The isolated whole crypts can be used to propagate long-lived and self-renewing 3D organoids in vitro.
FAQs
Persistent inflammatory signaling changes the behavior of intestinal fibroblasts and other stromal cells, shifting tissue repair toward sustained extracellular-matrix production. Transforming growth factor beta is important because it stimulates deposition of matrix components and collagen. This cellular response helps explain how inflammation can progress into structural remodeling and eventual loss of normal bowel function.
Fibroblasts and other stromal cells connect immune activity with physical changes in the intestinal wall. When persistent inflammation activates these cells, they participate in producing extracellular matrix and collagen rather than supporting limited repair alone. Their response therefore provides a cellular explanation for how prolonged immune signaling can contribute to fibrotic disease and bowel narrowing.
Normal repair is intended to restore tissue after injury, whereas persistent inflammatory signaling can maintain fibroblast and stromal-cell activity beyond the immediate repair period. In intestinal fibrosis, transforming growth factor beta promotes continued extracellular-matrix and collagen deposition. The resulting imbalance between repair and ongoing inflammation can produce structural changes that interfere with normal intestinal function.
Research should examine how immune responses, tissue-repair processes, intestinal fibroblasts, and other stromal cells influence one another during chronic inflammation. Connecting these cellular and molecular events can clarify why repair becomes associated with collagen and extracellular-matrix accumulation. This integrated view is especially relevant for understanding disease progression and the development of intestinal strictures.
By linking cellular signaling with changes in tissue structure, intestinal fibrosis research may identify indicators associated with disease progression. Relevant areas include persistent inflammation, activation of intestinal fibroblasts and stromal cells, transforming growth factor beta signaling, and extracellular-matrix or collagen deposition. Such biomarkers could help characterize progression toward strictures and improve assessment of fibrotic disease.
The topic provides a model for studying how immune responses and chronic inflammation interact with tissue repair. In this context, researchers can investigate how inflammatory signals activate stromal cells and promote collagen deposition, then relate those changes to bowel narrowing and impaired function. These findings may guide therapies designed to prevent or reverse intestinal strictures.