Free fucose is a danger signal to human intestinal epithelial cells.

Or equally (and much more likely) possible - the frucose capsule expressed by certain bacteroids fragilis binds with the same receptor (which is the intention of the expression of it in the first place) and causes the very same reaction.....................

"like dangling a lollipop in front of a kid" was what I believe I said about it.

I mentioned this on the last mucus thread. Map does this as well. But Fragilis being the UC bug of concern.

But then again - why would these guys ever think bacteria would be involved. It's always autoimmune, autoimmune, autoimmune. Actually not these guys, they're totally just pointing something out. So I can't get on them. Just they attribute it to dietary source.

Anyway. One more "fact" piece to add to the bacterial side on my end. Have quite the collection of facts and images now.

EDIT: Also it's a super interesting paper! So much to learn. Amazing all the stuff that goes on in side of us.

Post Edited (Canada Mark) : 11/10/2013 6:26:27 PM (GMT-7)

Yes, the bacteria do two things - First they "eat" the colon mucus so to speak, so they break down then internalize the frucose (from mucus) which becomes their source for external expression (of frucose) which allows them to adhere to epithelial cells via the sugar receptor on the cell. There's tons and tons on this when you start looking around.

I regards to adhesion; Have you ever tried daily Cranberry Juice?

I've been looking for goofy natural ways to maybe interfere and came across this finally a few minutes ago:

"This chapter provides a review of the various traditional approaches of antiadhesion therapy and immunity, including the use of adhesin-based vaccines, receptor and adhesin analogs, sub-lethal concentrations of antibiotics, dietary constituents, and innate host-derived antiadhesion factors. The adhesin analog strategy is based on the assumption that the isolated adhesin molecule or its synthetic or recombinant fragment binds to the receptor and thereby competitively blocks adhesion of the bacteria. It has so far been impractical to use adhesin analogs in antiadhesion therapy because they are almost always macromolecules that must be employed in relatively high molar concentrations and they are available only in limited supply. In addition, careful consideration must be given to their toxicity and immunogenicity. Nevertheless, modern proteomics and recombinant biotechnology have permitted the development of unique types of relatively small peptides for antiadhesion therapy. The chapter talks about the studies performed to investigate the antiadhesion activities of cranberry materials. In a study it was found that cranberry extract inhibited the coaggregation between pairs of gram-negative oral bacteria more often than it did those between pairs of gram-positive bacteria. The target of the antiadhesive activity is the bacterial adhesin, not the animal cell receptors or human mucus. The most important host-derived components which potentially may provide innate immunity by inhibiting adhesion are those found associated with mucus on mucosal surfaces. The secretor or nonsecretor status of individuals is of particular interest in relation to their susceptibility to infection and the possible role of soluble adhesin receptors."

I'm thinking while I'm at it I'll add a glass of cranberry Juice Daily. What heck.. One of these natural things has gotta work.. or all combined!

Whoa,huh what.

Citrate and many other compounds mimic fucose.

Now this might be scary.

OM

http://jvi.asm.org/content/86/1/284.full

cmr.asm.org/content/22/2/349.full.pdf+html

This one goes along with the above...

Point I'm trying to make is that I honestly think fragilis family bacteria is the "Ulcerative Colitis" version of an AIEC infection in Crohns.... So I have been collecting stuff to try and see if there's something to this - aside from just the visual confirmation in the 10,000 biopsy paper and a few others.

cid.oxfordjournals.org/content/38/12/1690.full.pdf+html

And one more.. sorry. But this highlights the confusion and problems in sampling as well as the confusion of what's going on - but obviously the same thing. Something's breaking down the mucus and bacteria are where they should not be in both Crohn's and Ulcerative Coitis.

Guess these should be on the mucus thread. but still.. The whole process seems eerily identical to AIEC in Crohn's but with different bacteria in Ulcerative Coitis.

Plus - well, more direct images of bacteria to add to the file. I just don't get how many times they have to actually "see" bacteria before they realize maybe these are causing the problem in the first place. Or targeting reduction in them for therapy rather than adjusting/dampening our immune response to them. I mean again, 40 years now they have been looking at them.. and doing nothing..

EDIT:

This particular paper ties back to the one I posted about the UC patient who had the perfectly normal left side colon and elected to have surgery to attach it to her rectum... a few months later wham... UC strikes the perfectly normal colon side and she ends up having the whole thing removed. It's as if the bacteria have made a home in the rectum and can travel up... So what's hiding out in the rectum of people with UC... And what's stopping them in the case of say right side and left side colitis. What's the actual difference here is what they should be looking at. It's the perfect twin study...

Post Edited (Canada Mark) : 11/11/2013 8:23:13 AM (GMT-7)

Here is something on FUT2. Messes with your gut bacteria and likely to get  to crohns.

OM

http://diabetes.diabetesjournals.org/content/60/11/2685.full

Well this one you posted was interesting.

Talks about the micro colonies, perhaps another term for biofilm,anyhow they would

have increased concentrations of bacterial products. 

Om

cid.oxfordjournals.org/content/38/12/1690.full.pdf+html

cel.webofknowledge.com/full_record.do?product=CEL&search_mode=CitingArticles&qid=1&Sid=2DJOKMHMBVknjy9Y4DE&pReturnLink=&pSrcDesc=&page=1&doc=8

So this sure changes all the mouse colon studies ... I wonder if his applies to humans as well. Just found it a second ago

Link didn't work: Here is the text.

A Crypt-Specific Core Microbiota Resides in the Mouse Colon


Source: MBIO Volume: 3 Issue: 3 Article Number: e00116-12 DOI: 10.1128/mBio.00116-12 Published:

MAY-JUN 2012
Times Cited: 2 (from Web of Science)

Cited References: 39

Abstract: In an attempt to explore the microbial content of functionally critical niches of the mouse gastrointestinal tract, we targeted molecular microbial diagnostics of the crypts that contain the intestinal stem cells, which account for epithelial regeneration. As current evidence indicates, the gut microbiota affects epithelial regeneration; bacteria that are likely to primarily participate in this essential step of the gut, microbiota cross talk, have been identified. We show in this article that only the cecal and colonic crypts harbor resident microbiota in the mouse and that regardless of the line and breeding origin of these mice, this bacterial population is unexpectedly dominated by aerobic genera. Interestingly, this microbiota resembles the restricted microbiota found in the midgut of invertebrates; thus, the presence of our so-called "crypt-specific core microbiota" (CSCM) in the mouse colon potentially reflects a coevolutionary process under selective conditions that can now be addressed. We suggest that CSCM could play both a protective and a homeostatic role within the colon. This article is setting the bases for such studies, particularly by providing a bona fide-and essentially cultivable-crypt microbiota of reference.

IMPORTANCE Metagenomic typing of the whole-gut luminal microbiome was recently provided, revealing great opportunities for physiological and physiopathological analysis of the host-microbiota interface. On this basis, it appears increasingly important to analyze which niches of the gut exposed to a particular microbiota are of major functional importance, specifically focusing on the crypt, which accounts for permanent epithelial renewal, and to analyze how this microbiota compares to its luminal counterpart in composition and quantity. Crypt-specific core microbiotas may show themselves as important elements regarding crypt protection and homeostasis of its functions.