What’s this all about? Yep it’s me using journalistic licence and I guess more towards the Gutter-press than high-brow stuff, I hear you say.
The microbiome (gut bacteria + other stuff) is at the centre of lots of MS research and here it is reported that a micro RNA (a small piece of genetic material) comming out of the Pooh when animals are sick and people with MS, cause then to make more certain types of bacteria in the gut and this stops EAE in Mice… So if it is important should post menopausal women stop exercising?
Plasma levels of miR-30d-5p are decreased in regularly exercising postmenopausal women.Kranjc T, Milojević M, Kocjan T, Jensterle M, Marc J, Ostanek B. Menopause. 2019 Oct 28. doi: 10.1097/GME.0000000000001454. [Epub ahead of print]
So if true does it mean we can use a pharmaceutical (micro RNA) rather than transplanting Pooh? Also why do the mice and humans get sick if they are making the magic ingredient?
Anyway something to get your teeth into.
It works by T regulatory cells. Now we have a million and one ways of makng T regs, what do they do in MS?, I hear you say.
If we got rid of T regs and it doesn’t get rid of MS…….then what should we do?
Oral Administration of miR-30d from Feces of MS Patients Suppresses MS-like Symptoms in Mice by Expanding Akkermansia muciniphila.Liu S, Rezende RM, Moreira TG, Tankou SK, Cox LM, Wu M, Song A, Dhang FH, Wei Z, Costamagna G, Weiner HL. Cell Host Microbe. 2019 Nov 12. pii: S1931-3128(19)30532-3.
Foecal transfer from healthy donors is being explored as a microbiome modality. MicroRNAs (miRNAs) have been found to affect the microbiome. Multiple sclerosis (MS) patients have been shown to have an altered gut microbiome. Here, we unexpectedly found that transfer of faeces harvested at peak disease from the experimental autoimmune encephalomyelitis (EAE) model of MS ameliorates disease in recipients in a miRNA-dependent manner. Specifically, we show that miR-30d is enriched in the faeces of peak EAE and untreated MS patients. Synthetic miR-30d given orally ameliorates EAE through expansion of regulatory T cells (Tregs). Mechanistically, miR-30d regulates the expression of a lactase in Akkermansia muciniphila (Gut mmicrobe), which increases Akkermansia abundance in the gut. The expanded Akkermansia in turn increases Tregs (Yeah T regs to the rescue…What don’t T regs do?) to suppress EAE symptoms. Our findings report the mechanistic underpinnings of a miRNA-microbiome axis and suggest that the faeces of diseased subjects might be enriched with miRNAs with therapeutic properties.