Hip
Senior Member
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I came across a very interesting study that may explain how mucosal viral infection could result in bacterial dysbiosis involving Enterococcus faecalis and Escherichia coli (the two most common bacteria Dr Markov finds in ME/CFS).
The study found when there is prolonged inflammation on the mucous membranes, this leads to overproduction of nitric oxide (NO).
The presence of high NO has a deleterious effect on the microbiome, depleting the beneficial butyrate-producing species, and promoting deleterious species like Enterococcus faecalis, Escherichia coli and Proteus mirabilis which are able to withstand high NO.
So elevated NO shifts the microbiome to undesirable bacterial species which can survive in high NO environments.
Now if the mucous membranes of ME/CFS patients are chronically infected with with viruses such as enterovirus, this may trigger chronic inflammation and NO production. So this could explain how viruses may trigger bacterial dysbiosis.
Possibly it may be feasible to reverse dysbiosis by inhibiting NO production on the mucous membranes. The NO produced by the immune system during inflammation is created by the enzyme inducible nitric oxide synthase (iNOS). So to reduce mucosal NO levels, an iNOS inhibitor might be effective.
Apparently aminoguanidine is a selective iNOS inhibitor, and this is available as a supplement.
On the other hand, this study found that in older mice, leaky gut was linked to low NO levels, the low NO levels caused by elevated arginase, an inhibitor of NO production. By giving the old mice an arginase inhibitor, they found this improves leaky gut.
The study found when there is prolonged inflammation on the mucous membranes, this leads to overproduction of nitric oxide (NO).
The presence of high NO has a deleterious effect on the microbiome, depleting the beneficial butyrate-producing species, and promoting deleterious species like Enterococcus faecalis, Escherichia coli and Proteus mirabilis which are able to withstand high NO.
So elevated NO shifts the microbiome to undesirable bacterial species which can survive in high NO environments.
Now if the mucous membranes of ME/CFS patients are chronically infected with with viruses such as enterovirus, this may trigger chronic inflammation and NO production. So this could explain how viruses may trigger bacterial dysbiosis.
Possibly it may be feasible to reverse dysbiosis by inhibiting NO production on the mucous membranes. The NO produced by the immune system during inflammation is created by the enzyme inducible nitric oxide synthase (iNOS). So to reduce mucosal NO levels, an iNOS inhibitor might be effective.
Apparently aminoguanidine is a selective iNOS inhibitor, and this is available as a supplement.
On the other hand, this study found that in older mice, leaky gut was linked to low NO levels, the low NO levels caused by elevated arginase, an inhibitor of NO production. By giving the old mice an arginase inhibitor, they found this improves leaky gut.
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