Multiple Sclerosis discovery could end disease's chronic inflammation
Fulltext:  <a href="https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3002000" rel="nofollow">https://journals.plos.org/plosbiology/article?id=10.1371/jou...</a>
Summary:<p>- Inflammation in experimental autoimmune encephalomyelitis (EAE), an animal model of MS, is driven to some extent by aryl hydrocarbon receptor (AHR) activation in the gut.<p>- AHR knockout mice are resistant to, or recover more swiftly from, EAE.<p>- An investigation of AHR knockout mice revealed that their microbiomes were different from normal mice in that they produce more bile acids of a certain type, as well as more of certain short-chain fatty acids.<p>- It was hypothesized that these metabolites, which enter circulation generally, alter the disease course of EAE, and affect susceptibility to EAE.<p>- Taurocholic acid, a bile acid that's available as an OTC drug in certain nations, was the most effective AHR-knockout-boosted-metabolite at suppressing EAE, when administered orally.  It is suggested as a potential treatment option for MS.<p>- The paper doesn't mention this, but taurocholic acid is hepatotoxic.  I believe it remains to be seen whether or not liver-safe bile acids are effective, e.g. tauroursodeoxycholic acid.