Just wondering if microbes that are more beneficial have more resistance to gut barrier defense systems
There was a recent paper on the resistance of commensal bacteria of the gut to host antimicrobial peptides due to LPS modification that might interest you. Here is a news story about it:
http://www.the-scientist.com/?articles.view/articleNo/41864/title/Commensal-Defense/
Adam, I just trolled your page and I noticed "Novel broad-spectrum inhibitors of bacterial methionine aminopeptidase," and methionine is one of the amino acid deficiencies in ALS patients. Any insight there?
I don't see a connection, but I'm open to suggestion. Methionine aminopeptidase cleaves off the N-terminal methionine residue from proteins. It is an essential enzyme in bacteria. It is also present in humans and is involved in angiogenesis.
https://en.wikipedia.org/wiki/METAP2
Perhaps you will also be interested in this: The assay I used to screen for inhibitors of methionine aminopeptidase included the enzyme S-adenosylmethionine (SAM) synthase for detecting the methionine produced by the cleavage reaction. SAM is an essential metabolite for many anabolic reactions in cells. It is made from methionine. I wonder what happens in methionine-deficient people to the level of SAM and the numerous biochemical reactions that depend upon it.
There is a functional mutation in that area involved in ALS, and when I read the paper on it, when the paper was written, it was the only known functional mutation... I think that is potentially a contributing mechanism in ALS, maybe due to nutritional deficiency...
I wonder if the methionine deficiencies are related to methylation issues that stop the homocysteine back to methionine. Some people with ALS are helped with betaine with the 3 methyl donors.
Looks like this step is a problem in ALS as well, Dr Tedone's Deanna Protocol is full of products from the transsulfuration pathway:
In liver cells (and only in liver cells) homocysteine can irreversibly enter the transsulfuration pathway (catalyzed by Vitamin B6) to produce the amino acid cysteine. It has been estimated that 60% of homocysteine is metabolized by transsulfuration in the liver, with glucocorticoids increasing that percentage [HUMAN MOLECULAR GENETICS; Ulrey,CL; 14:R139-R147 (2005)]. Cysteine can be incorporated into proteins, can be used in the formation of the anti-oxidant molecule glutathione (GSH), or can be oxidized to form the amino acid taurine.
http://www.benbest.com/health/Meth.html
If methionine or SAM deficiency caused by defective recycling of homocysteine to methionine is a cause of problems in ALS, would dietary supplementation with methionine be beneficial?
What are the potential problems that could arise from accumulation of homocysteine?
That would not reduce the high homocysteine.
Lots of problems with it raised, http://www.foodforthebrain.org/alzheimers-prevention/methylation-and-homocysteine.aspx
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