Effects of human marrow stromal cells on activation of microglial cells and production of inflammatory factors induced by lipopolysaccharide

Regulation of Mouse Microglia Activation and Effector Functions by Bone Marrow-Derived Mesenchymal Stem Cells

“…inflammatory (M1-like) into an anti-inflammatory (M2-like) phenotype [26,31,36] mainly through COX-2 mediated production of PGE2 and possibly some other soluble factors [35,37]. Similar PGE2-mediated interaction was also described between other tissue macrophages and MSCs in vitro [12], as well as in vivo [43].…”

“…However, the precise polarization states of microglia in the presence of MSCs under physiological or inflammatory conditions remain largely unknown. In most studies, xenogenic experimental systems were used; that is, cocultures of human MSCs with mouse or rat MGs [26,[31][32][33] and primary microglia were frequently replaced with neoplastic cell lines (BV2 or N9) [34][35][36] or with hippocampal slices [37]. Only two laboratories used autologous mouse [35] or rat [38] primary MGs and MSCs.…”

Mesenchymal Stem Cells Shape Microglia Effector Functions Through the Release of CX3CL1

“…Interestingly, MSC can induce dendritic cells to acquire a tolerogenic phenotype in vitro and in vivo [45] and educate alternatively activated macrophages [46] which have been demonstrated to be essential players in CNS healing [47]. Recently, Zhou et al [48] demonstrated that MSC are able to inhibit LPS-stimulated microglia activation and the production of inflammatory factors through diffusible molecules and, within an inflammatory environment, can significantly increase the production of neurotrophic factors, possibly involved in tissue repair. In addition, MSC exert neuroprotective effects on dopaminergic neurons via an antiinflammatory mechanism mediated by the modulation of microglia activation [49].…”

Beneficial effects of bone marrow-derived mesenchymal stem cell transplantation in a non-immune model of demyelination

“…In line with our results, several studies have been conducted to address the interaction between MSCs and microglia. Upon activation, microglia secrete a variety of inflammatory molecules that have been closely associated with the pathogenesis of MS. Zhou et al (2009) demonstrated that human MSCs sense inflammatory molecules that are released by activated microglia, thus significantly accelerating the secretion of neurotrophic factors, which are likely to be implicated in oligo/neuroprotection. Another potential mechanism to explain the increased survival of mature oligodendrocytes in transplanted mice is a direct inhibition of oligodendrocyte apoptosis.…”