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2025-01-01
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- IOC - Artigos de Periódicos [12967]
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MYCOBACTERIUM LEPRAE INDUCES NF-JB-DEPENDENT TRANSCRIPTION REPRESSION IN HUMAN SCHWANN CELLS
Hanseníase
Células Schwann
Talidomida
Repressão à transcrição
Leprosy
Mycobacterium leprae
Thalidomide
Transcription repression
Schwann
IjB-a;
p105
p65
p50
Author
Affilliation
Abstract
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.
Keywords in Portuguese
Mycobacterium lepraeHanseníase
Células Schwann
Talidomida
Repressão à transcrição
Keywords
NF-jBLeprosy
Mycobacterium leprae
Thalidomide
Transcription repression
Schwann
IjB-a;
p105
p65
p50
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