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NF-kappaB in the regulation of epithelial homeostasis and inflammation Wullaert A; Bonnet MC; Pasparakis MCell Res 2011[Jan]; 21 (1): 146-58The IkappaB kinase/NF-kappaB signaling pathway has been implicated in the pathogenesis of several inflammatory diseases. Increased activation of NF-kappaB is often detected in both immune and non-immune cells in tissues affected by chronic inflammation, where it is believed to exert detrimental functions by inducing the expression of proinflammatory mediators that orchestrate and sustain the inflammatory response and cause tissue damage. Thus, increased NF-kappaB activation is considered an important pathogenic factor in many acute and chronic inflammatory disorders, raising hopes that NF-kappaB inhibitors could be effective for the treatment of inflammatory diseases. However, ample evidence has accumulated that NF-kappaB inhibition can also be harmful for the organism, and in some cases trigger the development of inflammation and disease. These findings suggested that NF-kappaB signaling has important functions for the maintenance of physiological immune homeostasis and for the prevention of inflammatory diseases in many tissues. This beneficial function of NF-kappaB has been predominantly observed in epithelial cells, indicating that NF-kappaB signaling has a particularly important role for the maintenance of immune homeostasis in epithelial tissues. It seems therefore that NF-kappaB displays two faces in chronic inflammation: on the one hand increased and sustained NF-kappaB activation induces inflammation and tissue damage, but on the other hand inhibition of NF-kappaB signaling can also disturb immune homeostasis, triggering inflammation and disease. Here, we discuss the mechanisms that control these apparently opposing functions of NF-kappaB signaling, focusing particularly on the role of NF-kappaB in the regulation of immune homeostasis and inflammation in the intestine and the skin.|Animals[MESH]|Epithelial Cells/immunology/*metabolism[MESH]|Inflammation/immunology/*metabolism[MESH]|Intestines/cytology[MESH]|Mice[MESH]|NF-kappa B/*metabolism/physiology[MESH]|Signal Transduction[MESH] |
