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Published on: May 16, 2021
Elucidating a Myofibroblast-dominated Fibrotic Niche in Crohn's Disease-associated Fibrostenosis Through
Da Zhang1, Xinru Zou1, Mengjia He1
1Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Researchers identified submucosal myoid cells in Crohn's disease (CD) fibrostenosis as myofibroblasts originating from smooth muscle cells. This study highlights pericyte reprogramming and immune-stromal crosstalk, identifying key cell targets for antifibrotic therapies.
Area of Science:
- Gastroenterology
- Cell Biology
- Fibrosis Research
Background:
- Crohn's disease (CD) fibrostenosis involves intestinal remodeling and extracellular matrix (ECM) deposition.
- Submucosal myoid cell expansion and smooth muscle cell (SMC) hyperplasia are key features, but their origins and molecular drivers are unclear.
Purpose of the Study:
- To identify the cellular identity and molecular mechanisms of submucosal myoid cell hyperplasia in CD fibrostenosis.
- To delineate the cellular composition and spatial organization of the fibrotic niche in CD strictures.
Main Methods:
- Retrospective analysis of intestinal ultrasound and histological data from 117 CD patients.
- High-resolution spatial transcriptomics on fibrostenotic ileal tissue.
- Validation using single-cell RNA sequencing, immunofluorescence, and cell cultures.
Main Results:
- Submucosal myoid cells are primarily ECM-producing myofibroblasts originating from muscularis mucosae and submucosal vascular SMCs.
- Pericytes expand and reprogram into myofibroblast-like cells; FAP+ fibroblasts are enriched in fibrotic areas.
- Immune-stromal crosstalk occurs between inflammatory monocytes and stromal cells.
Conclusions:
- A spatially organized fibrotic niche in CD strictures comprises distinct stromal and immune cell populations.
- Profibrotic myofibroblast identity and origins are defined, along with pericyte reprogramming.
- Specific cell subtypes are identified as potential therapeutic targets for antifibrotic strategies in CD.
