Mechanism of steroid action in renal epithelial cells.

Abstract

Renal tubular epithelial cells (TEC) are thought to play an active role in tubulointerstitial inflammation. Various immune and non-immune factors activate TEC to produce a variety of cytokines and chemokines, contributing to attraction of inflammatory cells to the kidney. The proinflammatory transcription factor nuclear factor-kappaB (NF-kappaB) appears to be a key player in these responses and tubular expression of NF-kappaB has been demonstrated in vitro and in vivo. Although glucocorticoids are known to inhibit NF-kappaB activation at different levels, the proinflammatory capacity of TEC was not inhibited. In contrast, glucocorticoids seemed to enhance the profibrotic response of TEC, emphasizing the cell-type specific characteristics of glucocorticoid action. We propose that specific inhibition of NF-kappaB activation in TEC might be an attractive strategy for therapeutic intervention in renal inflammation.