Raw data to "Macrophage Plasticity and Polarization Are Altered in the Experimental Model of Multiple Sclerosis"

Background: Macrophages have been identified as one of the major effectors of inflammation and demyelination in both MS and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the activation and heterogeneity of macrophages in MS is not fully understood.

Results: We performed a complete immunophenotyping of M1 and M2 macrophages from EAE and control mice through polychromatic flow cytometry. We found that M1 macrophages possessed a higher proinflammatory profile in EAE compared to control mice, since they expressed higher levels of activation/co-stimulatory markers (iNOS, CD40 and CD80) (Table 1), cytokines/chemokines (IL-6, IL-12, CCL2 and CXCL10) (Table 2) and a higher expression of Toll-like receptors (TLR2) 2 and 5 (Table 3). On the contrary, M2 of EAE mice lost their M2-like phenotype by showing a decreased expression of their signature markers CD206, CD11c, CD44 and CCL22, and a concomitant upregulation of several M1 makers such as iNOS, CD40, CD80/CD86 (Table 1) and proinflammatory CCL22 (Table 2) and TLR4 and 8.

Conclusions: Our data account for a phenotypic alteration of M1/M2 balance during MS and this can be of crucial importance not only for a better understanding of the immunopathology of this neurodegenerative disease but also to potentially develop new macrophage-centered therapeutic strategies