The following is a summary of “Intestinal adipocytes transdifferentiate into myofibroblast-like cells and contribute to fibrosis in Crohn’s disease,” published in the March 2024 issue of Gastroenterology by Geng et al.
In Crohn’s disease (CD), while intestinal fat cells were previously shown to turn into scar-forming cells, researchers investigated their role in causing blockages in the intestines.
Researchers started a retrospective study investigating how intestinal fat cells contribute to scarring in the intestines of CD patients.
They analyzed changes in submucosal adipocytes in patients with CD with or without fibrotic stenosis (CDS or CDN) Crohn’s and individuals without the condition. Cell transdifferentiation into myofibroblasts and its contribution to fibrosis were examined, and human primary adipocytes and adipose organoids were used to investigate adipocyte transdifferentiation and fibrotic behavior. LPS/TLR4/TGF-β signaling involvement in this process was also explored.
The results showed a decrease or absence of submucosal adipocytes in tissue affected by CDS, with this decline showing a negative correlation with the severity of submucosal fibrosis. Adipocytes within CDS tissue underwent transdifferentiation into myofibroblast-like cells and expressed collagen components, possibly stimulated by bacteria translocated into the submucosa. LPS-stimulated human primary adipocytes and adipose organoids also underwent transdifferentiation and exhibited profibrotic behavior. Mechanistically, TLR4-mediated TGF-β signaling was associated with the transdifferentiation and profibrotic behavior of intestinal adipocytes in CDS tissue.
Investigators concluded that intestinal fat cells could transform into scar-forming cells and contribute to fibrosis in CD, likely through a specific signaling pathway.
Source: academic.oup.com/ecco-jcc/advance-article-abstract/doi/10.1093/ecco-jcc/jjae036/7625403