02081nas a2200397   4500000000100000008004100001260001600042653001200058653001400070653001700084653001100101653001900112653001200131653000900143653000900152653001500161653002300176653002500199653001800224653001200242653001800254653002400272100002300296700002600319700001200345700001800357700001200375700001900387700001600406700001100422245009800433300001300531490000800544520111700552022001401669       2010                            d  c2010 Oct 2910aAnimals10aApoptosis10aGangliosides10aHumans10aIntegrin beta110aleprosy10aMale10aMice10aMice, Nude10aModels, Biological10aMycobacterium leprae10aMyelin Sheath10aNeurons10aSchwann Cells10aSignal Transduction1 aRibeiro-Resende VT1 aRibeiro-Guimarães ML1 aLemes R1 aNascimento IC1 aAlves L1 aMendez-Otero R1 aPessolani M1 aLara F00aInvolvement of 9-O-Acetyl GD3 ganglioside in Mycobacterium leprae infection of Schwann cells.  a34086-960 v2853 a<p>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 suggest the involvement of 9-O-acetyl GD3 in ML infection on SCs.</p>  a1083-351X