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INVOLVEMENT OF 9-O-ACETYL GD3 GANGLIOSIDE IN MYCOBACTERIUM LEPRAE INFECTION OF SCHWANN CELLS
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Abstract
Mycobacterium leprae (ML), the etiologic agent of leprosy,
mainly affects the skin and peripheral nerves, leading to demyelization
and loss of axonal conductance. Schwann cells (SCs)
are the main cell population infected by ML in the nerves, and
infection triggers changes in the SC phenotype from a myelinated
to a nonmyelinated state. In the present study, we show
that expression of 9-O-acetyl GD3, a ganglioside involved in cellular
anti-apoptotic signaling and nerve regeneration, increases
in SCs following infection with ML. Observation by confocal
microscopy together with coimmunoprecipitation suggested
that this ganglioside participates in ML attachment and internalization
by SC. Immunoblockage of 9-O-acetyl GD3 in vitro
significantly reduced adhesion of ML to SC surfaces. Finally, we
show that activation of the MAPK (ERK 1/2) pathway and SC
proliferation, two known effects of ML on SCs that result in
demyelization, are significantly reduced when the 9-O-acetyl
GD3 ganglioside is immunoblocked. Taken together, these data
sugges.
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