期刊
PHARMACOLOGICAL RESEARCH
卷 177, 期 -, 页码 -出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2022.106056
关键词
Glucocorticoid; Intestinal barrier function; IgA; Colitis; Stress
资金
- Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain
- Ministry of Economy and Competitivity
- Fondo Europeo de Desarrollo Regional FEDER funds [SAF2017-88457-R, AGL2017-85270-R]
- Junta de Andalucia, Spain [CTS235, CTS164]
- Fondo de Investigaciones Sanitarias, Instituto de Salud Carlos III, Spain [PI19/00819]
- European Regional Development Fund/European Social Fund, Investing in your future
- Junta de Castilla y Leon, Spain [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 the effects of GCs on intestinal barrier function have received relatively little attention. This review summarizes the published studies on this matter and discusses the underlying mechanisms.
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.
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