Article
Mycobacterium leprae induces NF-jB-dependent transcription repression in human Schwann cells
Registro en:
PEREIRA, Renata M. S. et al. Mycobacterium leprae induces NF-jB-dependent transcription repression in human Schwann cells. Biochemical and Biophysical Research Communications, v. 335, p. 20-26, 2005.
0006-291X
10.1016/j.bbrc.2005.07.061
1090-2104
Autor
Pereira, Renata M. S.
Silva, Teresa Cristina Calegari
Hernandez, Maristela O.
Saliba, Alessandra M.
Redner, Paulo
Pessolani, Maria Cristina V.
Sarno, Euzenir N.
Sampaio, Elizabeth P.
Lopez, Ulisses G.
Resumen
Mycobacterium leprae, the causative agent of leprosy, invades peripheral nerve Schwann cells, resulting in deformities associated
with this disease. NF-jB is an important transcription factor involved in the regulation of host immune antimicrobial responses. We
aimed in this work to investigate NF-jB signaling pathways in the human ST88-14 Schwannoma cell line infected with M. leprae.
Gel shift and supershift assays indicate that two NF-jB 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 IjB-a degradation and
reduction of p105 levels. The nuclear translocation of p50/p50 complex due to M. leprae treatment correlated with repression of
NF-jB-driven transcription induced by TNF-a. Moreover, thalidomide inhibited p50 homodimer nuclear translocation induced
by M. leprae and consequently rescues Schwann cells from NF-jB-dependent transcriptional repression. Here, we report for the
first time that M. leprae induces NF-jB activation in Schwann cells and thalidomide is able to modulate this activation. 2025-01-01