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Thanks very much. There is not much news in the study but studies that confirm earlier findings are just as important. It's good to see confirmation that AIEC is surviving within macrophages and circumventing phagocytosis.
The suspicion that AIEC maintains a reservoir within tissue is supported by the fact people can go into full remission with clean scopes, and relapse with tissue damage within a few weeks. Those AIEC bacteria stay dormant for a while, and when they trigger lamina propria macrophages you get rapid tissue inflammation.
All bacteria in the intestine form biofilms, it's not that surprising that AIEC does this too. Phages can lyse AIEC, they penetrate these biofilms without any issues. These biofilms should be a non-issue with targeted treatment.
AIEC is resistant to many antibiotics, and will develop resistance over time, it's not a long-term solution. The most successful antibiotic therapies for CD have, not surprisingly, been those that are macrophage penetrating.
Phage therapy and anti-adhesive strategies like blocking FimH are possible solutions being developed to rid the intestine of AIEC.
Regarding the bacterial reservoir. Several researchers have long suspected that if crohn's disease is caused by a pathogen, there has to be a bacterial reservoir that would cause these chronic relapses.
Crohn's disease patients with full clinical healing, no dysbiosis, simply relapse a few months later. Why.
The intestine, but also the oral cavity, can serve as a bacterial reservoir. If the oral cavity served as a bacterial reservoir it might explain the aphthous ulcers seen in crohn's disease patients.
We still need to explain these aphthous ulcers in the mouths of people with crohn's disease, they are very common.
Kiny, is there an implication that a really robust dental hygiene routine is important in managing Crohn’s? And if so are there particular things that would control the E. coli reservoirs eg salt water gargle? Chlorhexidine mouthwash rather than a normal one?
@kiny@Pangolin If changing the diet (drastically) doesn't bring down the inflammation at all, is it reasonable to conclude that diet in this case is not the cause for Crohn's? By the same token, if the same diet change improves the inflammation #, can we claim that there is something else, in addition to the diet, that causes the inflammation?
So, like, A + B + C + D -> Crohn's so removing E doesn't help. And by observing the outcome of removing E we can get a glimpse of the formula.
One problem with that is that some causes aren't necessarily reversible. Take the mouse model of Crohn's with DSS. The mice are given DSS, and they get intestinal inflammation, but stopping the DSS doesn't stop the inflammation. Once the damage is there, other things need to be done to stop the inflammation. This possibility makes establishing causation much harder.