| Literature DB >> 29769726 |
Veit Rothhammer1, Davis M Borucki1, Emily C Tjon1, Maisa C Takenaka1, Chun-Cheih Chao1, Alberto Ardura-Fabregat2, Kalil Alves de Lima1, Cristina Gutiérrez-Vázquez1, Patrick Hewson1, Ori Staszewski2, Manon Blain3, Luke Healy3, Tradite Neziraj1, Matilde Borio1, Michael Wheeler1, Loic Lionel Dragin4, David A Laplaud5, Jack Antel3, Jorge Ivan Alvarez4, Marco Prinz2,6, Francisco J Quintana7,8.
Abstract
Microglia and astrocytes modulate inflammation and neurodegeneration in the central nervous system (CNS)1-3. Microglia modulate pro-inflammatory and neurotoxic activities in astrocytes, but the mechanisms involved are not completely understood4,5. Here we report that TGFα and VEGF-B produced by microglia regulate the pathogenic activities of astrocytes in the experimental autoimmune encephalomyelitis (EAE) mouse model of multiple sclerosis. Microglia-derived TGFα acts via the ErbB1 receptor in astrocytes to limit their pathogenic activities and EAE development. Conversely, microglial VEGF-B triggers FLT-1 signalling in astrocytes and worsens EAE. VEGF-B and TGFα also participate in the microglial control of human astrocytes. Furthermore, expression of TGFα and VEGF-B in CD14+ cells correlates with the multiple sclerosis lesion stage. Finally, metabolites of dietary tryptophan produced by the commensal flora control microglial activation and TGFα and VEGF-B production, modulating the transcriptional program of astrocytes and CNS inflammation through a mechanism mediated by the aryl hydrocarbon receptor. In summary, we identified positive and negative regulators that mediate the microglial control of astrocytes. Moreover, these findings define a pathway through which microbial metabolites limit pathogenic activities of microglia and astrocytes, and suppress CNS inflammation. This pathway may guide new therapies for multiple sclerosis and other neurological disorders.Entities:
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Year: 2018 PMID: 29769726 PMCID: PMC6422159 DOI: 10.1038/s41586-018-0119-x
Source DB: PubMed Journal: Nature ISSN: 0028-0836 Impact factor: 49.962