Molecular mechanisms of steroid resistance in chronic inflammatory bowel disease

摘要

Glucocorticoid resistance represents a serious clinical problem in various chronic inflammatory diseases, especially in chronic inflammatory bowel disease (IBD), asthma and rheumatoid arthritis. However, the molecular mechanisms underlying this steroid unresponsiveness are completely unknown. The effects of steroids result largely from the inhibition of pro-inflammatory transcription factors, such as NF-kB. Recently, increased activation of NF-kB in macrophages of the lamina propria from IBD patients has been reported1. Moreover, steroid treatment was associated with disappearance of active NF-kB in tissue from IBD patients2.