Adoptive Transfer of Immunomodulatory M2 Macrophages Suppresses
Experimental Autoimmune Encephalomyelitis in C57BL/6 Mice via Blockading
Objectives: The aims of the study were to further elucidate the roles of
M1 and M2 macrophages in the pathogenesis of EAE and the effects of
treatment with M2 macrophages that target certain pro-inflammatory
cytokines and with immunomodulatory preparations that beneficially
influence the disease course should be in focus of future therapeutic
trials. Results: Enhanced the total number of macrophages at the onset
of clinical signs in the EAE group, consistent with an increased
proportion of M1 cells and low numbers of M2 cells. As the disease
progressed and the symptoms worsened, M1 cells were decreased and M2
cells were gradually increased till the peak. In the recovery stage, M2
cell numbers were gradually decreased. Treatment with M2 macrophages
inhibited the NF-κb pathway, alleviated the symptoms of EAE, reduced
inflammatory cell infiltration and demyelination in the central nervous
system, and decreased the numbers of macrophages in the spleens.
BAY-11-7082, an NF-κb blocking agent, could reduce the total number of
macrophages both in vivo and in vitro, effectively prevented the EAE
development, and significantly inhibited the symptoms EAE in mice.
Conclusions: Macrophages may play a crucial role in the pathogenesis of
EAE, while M2 macrophages have anti-inflammatory effects. Transfer of M2
macrophages to EAE mice can block the NF-κb pathway successfully and
relieve the EAE symptoms. Application of NF-κb blockers is useful in the
prevention and treatment of EAE.