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Bone marrow cell transplant plays an immunomodulatory role in a reversible model of Wallerian degeneration in mice.

Gonzalo Miguel Piñero

  • CABA,
  • Argentina
  • Gonzalo Piñero ¹𝄒²
  • , Marianela Vence ²
  • , Marcos L. Aranda ³
  • , Magalí C. Cercato ²
  • , Paula A. Soto ¹𝄒²
  • , Vanina Usach ¹𝄒²
  • , Patricia Setton-Avruj ¹𝄒²
  • 1 Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Química Biológica, Cátedra de Química Biológica Patológica. Buenos Aires, Argentina.
  • 2 CONICET - Universidad de Buenos Aires, Instituto de Química y Fisicoquímica Biológicas (IQUIFIB). Buenos Aires, Argentina.
  • 3 CONICET - Universidad de Buenos Aires, Centro de Estudios Farmacológicos y Botánicos (CEFyBO). Buenos Aires, Argentina.

Initiated upon nervous system damage, Wallerian degeneration (WD) is a process characterized by axonal degeneration, demyelination and a strong inflammatory response. Working on a model of acute sciatic nerve lesion in rats, our group has shown the beneficial effects of systemic bone marrow mononuclear cell transplant on morphological and functional parameters, as well as the prevention of neuropathic pain. The current work thus seeks to further validate the experimental model in mice and aims to dig deeper into the mechanisms involved in bone marrow cell therapy.
Adult C57BL/6J mice were subjected to 8-sec sciatic nerve crush and immediately intravenously transplanted with bone marrow cells. The evolution of the degeneration-regeneration process was evaluated at different survival times. Gene and protein expression of the main cytokines involved in WD, as well as lesion-associated macrophage phenotypes, were also analyzed.
Initial findings corroborated the experimental model in mice but, most important, proved bone marrow cell efficiency in reducing the expression of some proinflammatory cytokines and increasing that of antiinflammatory IL-10. In addition, transplanted cells induced a decrease in iNOS+ macrophages at the expense of an increment in CD206+ cells and an anticipated rise in Arg-1+ macrophages. Taken together, our results endorse bone marrow cell therapy as an alternative approach to accelerate nerve recovery and postulate these cells as potential immunomodulator