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A microbial signature for Crohn's disease

A microbial signature for Crohn's disease

2017 Feb 7
  • Department of Gastroenterology, Barcelona, Spain
  • CIBERehd, Instituto de Salud Carlos III, Madrid, Spain
  • Department of Gastroenterology, University Hospital, Leuven, Belgium
  • Department of Gastroenterology, AP-HP, Hôpital Saint-Antoine, Paris, France
What this study shows is that Crohn's Disease and UC are very distinct diseases with no microbial overlap.

It also shows that Spanish, Belgian, UK and German Crohn's disease patients have high levels of pathogenic Fusobacterium and E Coli, which can be used as a diagnostic marker to help diagnose crohn's disease.

Patients with UC do not have either.
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What is interesting is that those bacterial profiles overlap strongly with small intestinal bacterial overload, especially in patients with stricturing disease. We also see that EN works by bringing down bacterial load in crohn's disease patients, EN works especially well in patients with stricturing disease.

The goal should be to bring down bacterial load to decrease bacterial antigen and to limit the fecal stream by increasing the biovailability of the diet like EN does.

The fact bacterial diversity goes down does not seem to matter, EN brings down bacterial diversity and seems to actually worsen the dysbiosis, but it greatly reduces bacterial antigen by a quick drop in bacterial load which leads to a rather significant drop in inflammation within a few days in patients.

All EN studies shows EN induces 'worsening' dysbiosis, a decrease in diversity, yet a rapid drop in inflammation due to a drop in bacterial load. The dysbiosis is also immediately reversed when people resume a 'normal' diet. This clearly shows dysbiosis itself is not the culprit behind the inflammation but the sheer amount of bacterial antigen interacting with the epithelial barrier and presence of pathogenic species in the lamina propria is behind the inflammation.

Studies have clearly shown that the fecal stream high in bacterial load induces the acute inflammation, and removing that fecal stream or limiting the fecal stream with EN leads to a quick drop in inflammation.

Crohn's disease is clearly not a reaction to the dysbiosis, but a reaction against high bacterial load of pathogenic species. E Coli, Fusobacterium, P mirabilis, these bacteria show highly pathogenic behavior in crohn's disease patients and are far more common in Crohn's disease than in HC or UC.
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The goal should also be to bring down bacterial load in the mouth, I have long argued that the oral cavity serves as a bacterial reservoir that potentially keeps reinfecting patients, because crohn's disease patients have aphthous ulcers. Recent studies have shown Campylobacter concisus might be chronically refinecting people by transporting those bacteria from the mouth, that serves as a reservoir, to the intestine.
It seems they are trying to use the microbiome to discriminate between other microbiomes and ibd, so these are the differences, but there are still similar extinct groups of bacteria in ibd types. This info might be good for assigning some diagnosis though, separate from the usual way they might discriminate between the ibd types, this is my best guess though. It could provide greater accuracy in diagnosis, and perhaps drug choices for therapy. the observation that the diversity in crohns is lower then uc could explain why FMT has been more effective in treating uc then crohns, as mouse studies have shown, the more damaged a microbiome is, the more it takes to correct it.
Im glad you are becoming more interested in the entire microbiome kiny, I know you have been focused on the role of AIEC.

I do recall the study on EN for crohns your are talking about, and this study may have been done at the beginning of establishing a science on the microbiome, so their description in a reduction of diversity as a good thing, may not have reflected an understanding of whether the microbiome was less diverse in good or bad microbes, but either way, disease activity seemed to be reduced anyways. This one observation of EN in CD may not contradict other observations that an increase of diversity in healthy microbes is strongly associated with better health. The patients could have experienced reductions in both pathogens and good bacteria, and still had reduced disease activity. They also may have simply had reduced disease activity due to getting of whatever their previous diet was, and didn't have much to do with the EN itself, so it isnt that EN is anything special its just that the patients previous diet was horrible.

Then there is the data we have that shows the people with the most improvements after FMT are the ones that acquired more of their donors microbiome then other patients, and an increase in diversity. So there are many observations of increased diversity that lead to better health in most cases.
You know my opinion on FMT for crohn's disease. The potential damage a FMT can do to crohn's disease patients is extensive due to the presence of peyer's patches and paneth cells, where stool high in bacterial load ends up entering tissue, like we have seen from the californian study that had to be halted. All FMT crohn's disease trials should have been halted after that study. Rutgeerts and follow up studies have shown that the fecal stream high in bacterial load leads to inflammation

Crohn's disease patients also have issues with tight junctions, the intestinal wall allows translocaton of bacteria deep into tissue, which is not the case in UC, the inflammation in crohn's disease is much more severe and transmural, extending deep into tissue, compared to UC.

The potential for a FMT to harm a crohn's disease patient is real, FMT in crohn's disease is now increasingly controversial and several voices in the research community have rightfully suggested halting FMT experiments in crohn's patients after the disastrous california trial where CRP, Calpotectrin and HBI showed extensive inflammation in several patients 2 days after FMT treatment (which matches Rutgeerts findings that the fecal stream will evoke an inflammatory response days after coming into contact with previously unaffected tissue).

Aministering supposedly "good" bacteria to crohn's disease patients with probiotics or other means is not feasable since the few that might be beneficial are oxygen sensitive, like Faecalibacterium prausnitzii. One can't administer this bacteria in any shape or form because it simply dies off in the presence of oxygen.

F prausnitzii counts also drop significantly when people use EN who go in remission, which again puts into question if certain bacteria are actually that beneficial as claimed.

Several types of Lactobacillus are able to halt the spread of E coli in a petri dish, but when administered to crohn's disease patients in the form of probiotics, it does not help, again, this puts into question this idea of "beneficial" bacteria for crohn's disease.

UC and C difficile are very different diseases exclusive to the colon where FMT seems to be effective. But a side-note, it is likely the bacteriophages that make the FMT effective, when you filter out the bacteria by using a 2um filter, the FMT is just as effective. The bacteriophages likely bring down the bacterial load in the colon.
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We also simply do not understand at all which bacteria live in the intestine and are present in stool. We have not identified the large majority of bacteria.

Fusobacterium was one of those bacteria that was intially cateogrized as harmless and even beneficial, only now do we understand this bacteria is a pathogen that enters tissue and caused an inflammatory response.

When certain doctors administer FMT to patients, they have no clue whatsoever what they are doing. These experiments are going to lead to disastrous outcomes, the californian study will not be the last where crohn's disease patients are actively harmed since the few voices in the research community that express worries and are asking for these experiments to stop in crohn's disease patients, are not listened to and science that shows the fecal stream evokes an immune response in crohn's disease patients is ignored.

It will not be until the FDA steps in and when patients start to sue these doctors harming them, or when another FMT leads to a dead patient, that the experiments will stop.

I thought that patients dying on FMT due to out of control E Coli and Salmonella infections would be enough for the research community to call out some of these doctors and hold them accountable. Apparently not, when all the scientific evidence shows the potential for harm, yet these doctors administered a FMT loaded with E Coli that ends up killing a patient, that doctor should be charged with murder and the wider research community has a responsibility to address these issues instead of trying to sweep them under a rug.
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