Bacteria links Crohn's disease to arthritis

"Patients with Crohn's disease, a type of inflammatory bowel disease (IBD) that causes abdominal pain and diarrhea, can also experience joint pain. In Crohn's disease, which affects about 800,000 Americans, the immune system can attack not only the bowels, but the musculoskeletal system as well, leading to spondyloarthritis, a painful condition that affects the spine and joints."

Link: /www.sciencedaily.com/releases/2017/02/170209133304.htm

I know there are many on here (both in UC forum and Crohns) with secondary joint pain issues.

Interesting. Thanks for sharing.

Thanks Mark: I think it is a chain of events.
Somehow we get a mucus breach, then inflammation.
What causes the initial breach, dont know.

In DSS colitis the mucus is dissolved or weakened or washed away.
The bacteria invade the mucosa, then after at least 12 hours immune cells show up.
Then as I always say, after this insult to the colon, if the DSS is stopped the mice get better.
Why do they get better and we dont.

So for humans perhaps part genetic/epigenitc, or something else we are eating.
Another question is why us, and not also everyone else,which might bring us back to genetics again.

Once the inflammation starts, and we have killed off many anaerobes due to oxygen tension/
ROS/nitrates, the whole ecosystem is disturbed.

Getting back to your interesting paper again.
Looks like there is an aerobic switch going on here.

Old Mike

OXIDATIVE GLUCOSE METABOLISM
The discovery of a pyrroloquinoline quinone (PQQ)-dependent glucose dehydrogenase, which catalyzes the oxidation of glucose to gluconate (Fig. ​(Fig.1)1) in the periplasm, suggested an alternate route for glucose catabolism in E. coli (33). Mutants defective in enzyme I of the PTS are able to grow on glucose in the presence of exogenous PQQ (16). Paradoxically, wild-type E. coli does not synthesize PQQ (43). Results showed that under aerobic, but not anaerobic, conditions functional glucose dehydrogenase allowed growth on glucose of double mutants blocked at phosphoglucose isomerase and glucose-6-phosphate dehydrogenase (1). Subsequent experiments provided direct evidence that the ED pathway is turned on by oxidation of glucose to gluconate in the periplasm (27). The oxidative glucose pathway might be important for survival of E. coli in aerobic, aquatic environments. Similarly, Klebsiella pneumoniae and Pseudomonas aeruginosa preferentially oxidize as much as 80% of the glucose they consume to gluconate, which is catabolized via the ED pathway (34, 41).

il-23 is what is targeted by Stelara/Ustekinumab
I know from my 23andme test that I have that gene implicated, in their outdated list of risk genes for UC it is one. I wish I could afford to try Stelara, not licensed in the UK for UC as yet too expensive on private.

Must look up your links to see if anything "natural" can target it

Thank you OM. Grapefruit is a no no on my current med. I'm on high dose D at the moment too.
Pomegranate is a new one on me, will have to look that up.

Lets go down a slightly different path with pomegranate, I have eaten fresh in the past dont
remember any improvement, but never the less.


increases Akkermansia muciniphila
/www.ncbi.nlm.nih.gov/pubmed/26189645

cranberry
/www.ncbi.nlm.nih.gov/pubmed/26900906

this is a mucin degrading bacteria depleted in UC and crohns
/www.ncbi.nlm.nih.gov/pubmed/26875998

more
/www.ncbi.nlm.nih.gov/pubmed/23385241

other mucin2 degrading bacteria seem to be upregulated in UC
/www.ncbi.nlm.nih.gov/pubmed/20648002

perhaps a healing mechanism
/www.ncbi.nlm.nih.gov/pubmed/26849730

Seems odd that we might have lost a mucin degrading bacteria,yet it seems
that increasing it might lead to healing,via immune cross talk, and inhibition of
other mucin degrading bacteria.
Perhaps FMT restores some of these.

Here is an old thread where the OP seems to do well with pomegranate.

www.healingwell.com/community/default.aspx?f=38&m=3520583

Old Mike