Details

Autor(en) / Beteiligte

• Hoban, Alan
• Stilling, Roman
• Desbonnet, Lieve
• Shanahan, Fergus
• Dinan, Timothy
• Cryan, John
• Clarke, Gerard

Titel

Regulation of Myelination in the Prefrontal Cortex by the Gut Microbiota: Implications for Health and Disease

Ist Teil von

• The FASEB journal, 2015-04, Vol.29 (S1)

Erscheinungsjahr

2015

Link zum Volltext

Quelle

Wiley-Blackwell Journals

Beschreibungen/Notizen

• Abstract only Background Multiple lines of evidence suggest a potential role for the gut microbiome in multiple sclerosis, a degenerative demyelinating disorder. For example, germ‐free mice, which are microbiota deficient, appear to be protected against the development of experimental allergic encephalomyelitis (EAE). The gut microbiota can regulate gene expression at the level of the CNS. In this study, we aimed to establish whether germ‐free mice have alterations in genes of relevance to CNS myelination. Methods Using qRT‐PCR, we evaluated expression levels of myelin basic protein (Mbp), myelin oligodendrocyte protein (Mog), myelin oligodendrocyte basic protein (Mobp), proteolipid protein 1 (Plp1) and myelin associated glycoprotein (Mag) in relevant brain regions in conventionally raised, germ‐free and germ‐free colonised mice. Results Germ‐free mice displayed increased expression of all 5 myelinating genes only within the prefrontal cortex. Colonisation of the germ‐free animals immediately post‐weaning normalised the expression of these myelin structural protein genes. Germ‐free mice also displayed a 2 fold increase in expression of Egr2/Krox20, a transcription factor within the PFC known to be involved in mechanisms regulating myelin formation. Conclusion The gut microbiota can regulate myelin structural protein gene expression in the CNS. Moreover, our results suggest that the microbiota can be successfully targeted later in life to modulate myelination patterns. This raises the possibility that targeting the gut microbiota during critical time windows could be a viable approach to promote remyelination or to prevent further demyelination in disorders such as multiple sclerosis.