Modulation of intestinal barrier function by glucocorticoids: Lessons from preclinical models
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AuthorTena Garitaonaindia, Mireia; Arredondo Amador, María; Mascaraque Molina, Cristina; Martínez Augustín, María Olga; Sánchez De Medina López-Huertas, Fermín
GlucocorticoidIntestinal barrier functionIgAColitisStress
Mireia Tena-Garitaonaindia... [et al.]. Modulation of intestinal barrier function by glucocorticoids: Lessons from preclinical models, Pharmacological Research, Volume 177, 2022, 106056, ISSN 1043-6618, [https://doi.org/10.1016/j.phrs.2022.106056]
Sponsorship"Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain; Ministry of Economy and Competitivity; European Commission SAF2017-88457-R AGL2017-85270-R; Junta de Andalucia European Commission CTS235 CTS164; Instituto de Salud Carlos III PI19/00819; European Regional Development Fund/European Social Fund, "Investing in your future"; Junta de Castilla y Leon SA074P20; Fundacio Marato TV3, Spain 201916-31; AECC Scientific Foundation, Spain; "Centro Internacional sobre el Envejecimiento" (OLD-HEPAMARKER), Spain 0348_CIE_6_E; Ministry of Education; CIBERehd; Universidad de Granada/CBUA
Glucocorticoids (GCs) are widely used drugs for their anti-inflammatory and immunosuppressant effects, but they are associated with multiple adverse effects. Despite their frequent oral administration, relatively little attention has been paid to the effects of GCs on intestinal barrier function. In this review, we present a summary of the published studies on this matter carried out in animal models and cultured cells. In cultured intestinal epithelial cells, GCs have variable effects in basal conditions and generally enhance barrier function in the presence of inflammatory cytokines such as tumor necrosis factor (TNF). In turn, in rodents and other animals, GCs have been shown to weaken barrier function, with increased permeability and lower production of IgA, which may account for some features observed in stress models. When given to animals with experimental colitis, barrier function may be debilitated or strengthened, despite a positive anti-inflammatory activity. In sepsis models, GCs have a barrier-enhancing effect. These effects are probably related to the inhibition of epithelial cell proliferation and wound healing, modulation of the microbiota and mucus production, and interference with the mucosal immune system. The available information on underlying mechanisms is described and discussed.