@misc{10481/76482,
year = {2021},
month = {3},
url = {http://hdl.handle.net/10481/76482},
abstract = {Intestinal epithelium glucocorticoid receptor knockout mice (NR3C1 IEC) were treated
with dextran sulfate sodium (DSS, 2.5%) to induce colitis. Inflammatory status was
assessed by morphological and biochemical methods and corticoid production was
measured in colonic explants.
Key Results.
After 7 days of DSS NR3C1 mice exhibited lower weight loss and tissue damage,
reduced colonic expression of S100A9, attenuated phosphorylation of STAT3 and a better
overall state compared with WT. Ki67 immunoreactivity was also shifted, indicating an
effect on epithelial proliferation. A subgroup of mice were treated with budesonide and
showed completely prevented budesonide induced weight loss. Epithelial deletion of the
glucocorticoid receptor also protected mice in a protracted colitis protocol. Conversely
knockout mice presented a worse status compared to the control group at 1 day post DSS,
as shown by blood in feces and increased inflammatory parameters. In a separate
experiment colonic corticosterone production was shown to be significantly increased in
knockout mice at 7 days of colitis but not at earlier stages.
Conclusions and Implications.
The intestinal epithelial glucocorticoid receptor has deleterious effects in experimental
colitis induced by dextran sodium sulfate, probably related to inhibition of epithelial
proliferative responses leading to impaired wound healing and reduced endogenous
corticosterone production.},
organization = {Ministry of Economy and Competitivity, partly with Fondo Europeo de Desarrollo Regional FEDER funds [BFU2014-57736-P, AGL2014-58883-R, SAF2017-88457-R, AGL2017-85270-R]},
organization = {Junta de Andalucía [CTS235, CTS164]},
organization = {Ministry of Education},
organization = {CIBERehd is funded by Instituto de Salud Carlos III},
publisher = {The British Pharmacological Society},
keywords = {Glucocorticoids},
keywords = {Budesonide},
keywords = {Epithelium},
keywords = {Intestinal barrier function},
title = {Epithelial deletion of the glucocorticoid receptor protects the mouse intestine against experimental inflammation},
doi = {10.1111/bph.15434},
author = {Sánchez De Medina López-Huertas, Fermín and Martínez Augustín, María Olga and Arredondo Amador, María and Aranda, Carlos J. and Ocón, Borja and González Pérez, Raquel},
}