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김성근,김영미,염정은,진송효,채규태,이성범 대한약리학회 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.6
Rifampicin is a macrocyclic antibiotic which is used extensively for treatment against Mycobacterium tuberculosis and other mycobacterial infections. Recently, a number of studies have focused on the immune-regulatory effects of rifampicin. Therefore, we hypothesized that rifampicin may influence the TLR2 expression in LPS-activated RAW 264.7 cells. In this study, we determined that rifampicin suppresses LPS-induced TLR2 mRNA expression. The down-regulation of TLR2 expression coincided with decreased production of TNF-α. Since NF-κB is a major transcription factor that regulates genes for TLR2 and TNF-α, we examined the effect of rifampicin on the LPS-induced NF-κB activation. Rifampicin inhibited NF-κB DNA-binding activity in LPS-activated RAW 264.7 cells, while it did not affect IKKα/β activity. However, rifampicin slightly inhibited the nuclear translocation of NF-κB p65. In addition, rifampicin increased physical interaction between pregnane X receptor, a receptor for rifampicin, and NF-κB p65, suggesting pregnane X receptor interferes with NF-κB binding to DNA. Taken together, our results demonstrate that rifampicin inhibits LPS-induced TLR2 expression, at least in part, via the suppression of NF-κB DNA-binding activity in RAW 264.7 cells. Thus, the present results suggest that the rifampicin-mediated inhibition of TLR2 via the suppression of NF-κB DNA- binding activity may be a novel mechanism of the immune-suppressive effects of rifampicin.