Obesity activates immunomodulating properties of mesenchymal stem cells in adipose tissue with differences between localizations
Abstract
Mesenchymal stem cells from healthy adipose tissue are adipocytes progenitors with immunosuppressive potential that are used for years in cell therapy. Whether adipose stem cells (ASC) may prevent inflammation in early obesity is not known. To address this question, we performed a kinetic study of high-fat (HF) diet induced obesity in mice to follow the immune regulating functions of adipose stem cells (ASC) isolated from the subcutaneous (SAT) and the visceral adipose tissue (VAT). Our results show that, early in obesity and before inflammation was detected, HF diet durably and differently activated ASC from SAT and VAT. Subcutaneous ASC from HF-fed mice strongly inhibited the proliferation of activated T lymphocytes, whereas visceral ASC selectively inhibited TNF alpha expression by macrophages and simultaneously released higher concentrations of IL6. These depot specific differences may contribute to the low-grade inflammation that develops with obesity in VAT while inflammation in SAT is delayed. The mechanisms involved differ from those already described for naive cells activation with inflammatory cytokines and probably engaged metabolic activation. These results evidence that adipose stem cells are metabolic sensors acquiring an obesity-primed immunocompetent state in answer to depot-specific intrinsic features with overnutrition, placing these cells ahead of inflammation in the local dialog with immune cells.
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BibTeX
@article{lefevre2026obesity,
title = {{Obesity activates immunomodulating properties of mesenchymal stem cells in adipose tissue with differences between localizations}},
author = {Camille Lefevre and Dimitri Chartoire and Jose Candido Ferraz and Thomas Verdier and Claudie Pinteur and Stéphanie Chanon and Sandra Pesenti and Aurélie Vieille‐marchiset and Laurent Genestier and Hubert Vidal and Anne Mey},
journal = {FASEB Journal},
year = {2026},
month = oct,
doi = {10.1096/fj.202002046rr},
url = {https://hal.inrae.fr/hal-03331272v1},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Obesity activates immunomodulating properties of mesenchymal stem cells in adipose tissue with differences between localizations
AU - Camille Lefevre
AU - Dimitri Chartoire
AU - Jose Candido Ferraz
AU - Thomas Verdier
AU - Claudie Pinteur
AU - Stéphanie Chanon
AU - Sandra Pesenti
AU - Aurélie Vieille‐marchiset
AU - Laurent Genestier
AU - Hubert Vidal
AU - Anne Mey
PY - 2026
DA - 2026/10/05
JO - FASEB Journal
DO - 10.1096/fj.202002046rr
UR - https://hal.inrae.fr/hal-03331272v1
AB - Mesenchymal stem cells from healthy adipose tissue are adipocytes progenitors with immunosuppressive potential that are used for years in cell therapy. Whether adipose stem cells (ASC) may prevent inflammation in early obesity is not known. To address this question, we performed a kinetic study of high-fat (HF) diet induced obesity in mice to follow the immune regulating functions of adipose stem cells (ASC) isolated from the subcutaneous (SAT) and the visceral adipose tissue (VAT). Our results show that, early in obesity and before inflammation was detected, HF diet durably and differently activated ASC from SAT and VAT. Subcutaneous ASC from HF-fed mice strongly inhibited the proliferation of activated T lymphocytes, whereas visceral ASC selectively inhibited TNF alpha expression by macrophages and simultaneously released higher concentrations of IL6. These depot specific differences may contribute to the low-grade inflammation that develops with obesity in VAT while inflammation in SAT is delayed. The mechanisms involved differ from those already described for naive cells activation with inflammatory cytokines and probably engaged metabolic activation. These results evidence that adipose stem cells are metabolic sensors acquiring an obesity-primed immunocompetent state in answer to depot-specific intrinsic features with overnutrition, placing these cells ahead of inflammation in the local dialog with immune cells.
SN - 0892-6638
SN - 1530-6860
ER -