Mycobacterium leprae induces NF-κB-dependent transcription repression in human Schwann cells
- 作者：Renata M.S. Pereira ; Teresa Cristina Calegari-Silva ; Maristela O. Hernandez ; Alessandra M. Saliba ; Paulo Redner ; Maria Cristina V. Pessolani ; Euzenir N. Sarno ; Elizabeth P. Sampaio and Ulisses G. Lope
- 关键词：NF-κ ; B ; Leprosy ; Mycobacterium leprae ; Thalidomide ; Transcription repression ; Schwann ; Iκ ; B-α ; p105 ; p65 ; p50
- 刊名：Biochemical and Biophysical Research Communications
- 出版年：2005
- 期刊代码：159_0006291x
- 类别：bio
- 出版时间：2005
- 卷：335
- 期：1
- 页码：20-26
- 文件大小：628 K
摘要
Mycobacterium leprae, the causative agent of leprosy, invades peripheral nerve Schwann cells, resulting in deformities associated with this disease. NF-κB is an important transcription factor involved in the regulation of host immune antimicrobial responses. We aimed in this work to investigate NF-κB signaling pathways in the human ST88-14 Schwannoma cell line infected with M. leprae. Gel shift and supershift assays indicate that two NF-κB dimers, p65/p50 and p50/p50, translocate to the nucleus in Schwann cells treated with lethally irradiated M. leprae. Consistent with p65/p50 and p50/p50 activation, we observed IκB-α degradation and reduction of p105 levels. The nuclear translocation of p50/p50 complex due to M. leprae treatment correlated with repression of NF-κB-driven transcription induced by TNF-α. Moreover, thalidomide inhibited p50 homodimer nuclear translocation induced by M. leprae and consequently rescues Schwann cells from NF-κB-dependent transcriptional repression. Here, we report for the first time that M. leprae induces NF-κB activation in Schwann cells and thalidomide is able to modulate this activation.