Diarrhea-causing bacteria promote growth of Crohn's-linked microbe in mice
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kiny
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Thank you. Here is a list of AIEC studies: http://www.crohnsforum.com/showthread.php?t=52198
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And here's the full publication:
http://journals.plos.org/plospathog...ns/NewArticles+(PLOS+Pathogens+-+New+Articles)
Just to add a bit more,cellulose might be a bad actor. Looks like
all fiber is not created equal, and we know there is a lot of CMC
used as a food additive.
http://www.jimmunol.org/content/196/1_Supplement/67.11
AIEC generates its own cellulose.
http://iai.asm.org/content/83/10/4068.full
now this is also very interesting on enteral feeding, the guy
was fine after remission induced by enteral feeding, then went on
a regular diet minus veggies, when he started veggies relapsed.
This was a 4 year trial on a one person sample.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1378894/
Another mystery is how can enteral feeding put crohns into remission, yet when a normal
diet is restarted the disease progresses. The last time I searched it years ago the answer was at that time unknown.
Wow strictures and veggie residue seemed to cause the relapse.
Brussel sprouts,carrots,onions,cauliflower and green beans were added.
A possible connection might be that it is just cellulose getting stuck and growing bacteria,
humans don't have cellulase or very little,so cullulose cant be digested in the small intestine.
Old Mike
all fiber is not created equal, and we know there is a lot of CMC
used as a food additive.
http://www.jimmunol.org/content/196/1_Supplement/67.11
AIEC generates its own cellulose.
http://iai.asm.org/content/83/10/4068.full
now this is also very interesting on enteral feeding, the guy
was fine after remission induced by enteral feeding, then went on
a regular diet minus veggies, when he started veggies relapsed.
This was a 4 year trial on a one person sample.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1378894/
Another mystery is how can enteral feeding put crohns into remission, yet when a normal
diet is restarted the disease progresses. The last time I searched it years ago the answer was at that time unknown.
Wow strictures and veggie residue seemed to cause the relapse.
Brussel sprouts,carrots,onions,cauliflower and green beans were added.
A possible connection might be that it is just cellulose getting stuck and growing bacteria,
humans don't have cellulase or very little,so cullulose cant be digested in the small intestine.
Old Mike
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there was a study that studied the microbiota under enteral feeding and shown that the "diversity" of bacteria declined, not sure if they were able to determine if it was a diversity in good or bad bacteria, but they did connect a certain species to the reduction of inflammation. The carbohydrate used was maltodextrin supposedly its a polysaccharide and not a simple sugar but supposedly quickly turned into glucose, my best guess is that by providing a lack of diverse carbs/fibers etc, this would lead to a reduction in diverse pathogens that could otherwise utilize them for growth.
Old Mike[/QUOTE]
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One of the two products they used in the trial was this:
Elemental 028 Extra Powder
http://nutricia.co.uk/e028/products/e028_extra_powder
http://nutricia.co.uk/e028/uploads/Elemental_028_Extra_Powder_Datacard.pdf
It doesn't have maltodextrin and carageenan, and it is good for people who have sensitivities to milk based whole proteins (like casein, whey).
They also have a liquid form enteral feeding product; but it has maltodextrin in it.
here:
Elemental 028 Extra Liquid
http://nutricia.co.uk/e028/products/e028_extra_liquid
I think the powder is really a good alternative to Modulen. For example, I can't use modulen because of my problems with casein. It puts me into a flare.
kiny
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There's multiple things required for AIEC colonization. You need the actual bacteria, AIEC, found in many people with CD, but also in a number without CD. Regular non-pathogenic E. Coli do not bind to epithelial cells, it does not invade the intestine, they're harmless commensal bacteria. AIEC are not, but they need a specific molecule to adhere to and invade epithelial cells, specifically ileal enterocyte, AIEC's forte is the ileum. That molecule is called CEACAM6, AM stands for adhesion molecule. CEACAM6 is seen a lot in patients with CD, not nearly as much in patients without CD.
One theory is that, not only AIEC uses CEACAM6, but the body can also use soluble CEACAM6 as a decoy binding protein preventing AIEC from invading the intestine. And for some reason, EN formulas, increase the amount of soluble CEACAM6 that are released.
There's also been a good study that showed that EN exclusivity is not why EN seems to help some people with CD. EN in addition to a normal diet gave the same results. So it's not the absence of X or Y in a normal diet that is of importance when taking EN, EN itself seems to help people for some reason.
It also doesn't hurt that EN formulas like 028 and Modulen contain all the nutrients people need, diverse amino acid profile, glutamine used extensively by the small intestine, vitamins like B12 and vitamin D, which tend to be lacking in people with CD, etc.
One theory is that, not only AIEC uses CEACAM6, but the body can also use soluble CEACAM6 as a decoy binding protein preventing AIEC from invading the intestine. And for some reason, EN formulas, increase the amount of soluble CEACAM6 that are released.
There's also been a good study that showed that EN exclusivity is not why EN seems to help some people with CD. EN in addition to a normal diet gave the same results. So it's not the absence of X or Y in a normal diet that is of importance when taking EN, EN itself seems to help people for some reason.
It also doesn't hurt that EN formulas like 028 and Modulen contain all the nutrients people need, diverse amino acid profile, glutamine used extensively by the small intestine, vitamins like B12 and vitamin D, which tend to be lacking in people with CD, etc.
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Seems that AIEC might also be implicated in UC.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133521/
Inhibitors of adhesion so far that we can get are Danactive with a particular strain of L casei DN-114 001 , but cant
seem to find Danactive at any store sites anymore, did they stop selling it. Still seems to be on the Dannon site.
Also cant seem to find that strain anywhere else.
Also genistein, which you can get as a supplement, but it may be estrogenic.
Many strains are also mannose resistant.
One mechanism they use is that they are highly hydrophobic, which lowers their surface charge, which lowers repulsion.
Always thought AIEC was just involved with crohn's, from the above paper, perhaps not.
Maltodextrin seems to promote it as does polysorbate 80, there is also a seaweed compound that repels it.
Old Mike
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133521/
Inhibitors of adhesion so far that we can get are Danactive with a particular strain of L casei DN-114 001 , but cant
seem to find Danactive at any store sites anymore, did they stop selling it. Still seems to be on the Dannon site.
Also cant seem to find that strain anywhere else.
Also genistein, which you can get as a supplement, but it may be estrogenic.
Many strains are also mannose resistant.
One mechanism they use is that they are highly hydrophobic, which lowers their surface charge, which lowers repulsion.
Always thought AIEC was just involved with crohn's, from the above paper, perhaps not.
Maltodextrin seems to promote it as does polysorbate 80, there is also a seaweed compound that repels it.
Old Mike
kiny
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They sell those little bottles with sugary milk from Danone and their L Casei strain in most grocery stores in Europe.
AIEC colonization in mice requires a trigger event, antibiotics or an infection with a foodborne bacteria.
This reminds me of the cold chain hypothesis, people started freezing food and started to use personal refrigerators at the same time crohn's disease started to become widespread.
https://www.ncbi.nlm.nih.gov/pubmed/14683664
Unlike most bacteria, AIEC thrives in an inflammatory environment. It circumvents the innate immune system and replicates inside macrophages and the more cytokine get released, the more CEACAM6 molecules it has available.
And like you said, it uses a type of biofilm, which makes it very hard for antibiotics to target it. And one has to be very careful with some antibiotics, since broad spectrum antibiotics might make it much easier for AIEC to colonize since a lot of the resident commensal bacteria are removed. I believe some people respond temporarily to cipro since it's one of the more effective antibiotics against those E Coli strains, but inevitably you'll run into resistance and you might be worse off than before you started the regimen, since lots of those commensals will have been killed too.
This is also why I've been hesitant about those anti-MAP treatments based on 3 antibiotics. One has to be 100% confident that that person's inflammation is being caused by MAP and that that person harbors MAP. They're broad spectrum antibiotics that are not specifically targetting gram negative bacteria, and could potentially make the disease worse just like in those mice that are colonized by AIEC right after antibiotics use. Several studies also suggested that antibiotics use might be linked to crohn's disease in some people.
AEIC is also incredibly antibiotics resistant. http://www.crohnsforum.com/showthread.php?t=39306
"AIEC strains from ICD (6/8 patients) versus 2/6 NI (2/5 patients) showed resistance to the macrophage-penetrating antimicrobials ciprofloxacin, clarithromycin, rifampicin, tetracycline, and trimethoprim/sulfamethoxazole."
It's a very nasty bacteria.
AIEC colonization in mice requires a trigger event, antibiotics or an infection with a foodborne bacteria.
This reminds me of the cold chain hypothesis, people started freezing food and started to use personal refrigerators at the same time crohn's disease started to become widespread.
https://www.ncbi.nlm.nih.gov/pubmed/14683664
Unlike most bacteria, AIEC thrives in an inflammatory environment. It circumvents the innate immune system and replicates inside macrophages and the more cytokine get released, the more CEACAM6 molecules it has available.
And like you said, it uses a type of biofilm, which makes it very hard for antibiotics to target it. And one has to be very careful with some antibiotics, since broad spectrum antibiotics might make it much easier for AIEC to colonize since a lot of the resident commensal bacteria are removed. I believe some people respond temporarily to cipro since it's one of the more effective antibiotics against those E Coli strains, but inevitably you'll run into resistance and you might be worse off than before you started the regimen, since lots of those commensals will have been killed too.
This is also why I've been hesitant about those anti-MAP treatments based on 3 antibiotics. One has to be 100% confident that that person's inflammation is being caused by MAP and that that person harbors MAP. They're broad spectrum antibiotics that are not specifically targetting gram negative bacteria, and could potentially make the disease worse just like in those mice that are colonized by AIEC right after antibiotics use. Several studies also suggested that antibiotics use might be linked to crohn's disease in some people.
AEIC is also incredibly antibiotics resistant. http://www.crohnsforum.com/showthread.php?t=39306
"AIEC strains from ICD (6/8 patients) versus 2/6 NI (2/5 patients) showed resistance to the macrophage-penetrating antimicrobials ciprofloxacin, clarithromycin, rifampicin, tetracycline, and trimethoprim/sulfamethoxazole."
It's a very nasty bacteria.
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kiny
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It's also a question of some stubborn GI who don't want to re-educate themselves. You still have these GI who refuse to believe that crohn's disease is in any way related to bacteria.
Every genetic predisposition in crohn's disease, NOD2, ATG16L1, vitamin D receptors, IL-23....every single one is related to recognition of bacteria and innate and autophagy response to bacteria, every single one.
NOD2 is required for autophagy induction during AIEC infections: https://www.ncbi.nlm.nih.gov/pubmed/27335178.
When you give a crohn's disease patient an antibiotic for an unrelated infection, this could have serious consequences on their disease and the proliferation of AIEC or other bacteria, they need to know this. But if you have a GI who still thinks crohn's disease is some autoimmune disease, they don't think antibiotics affect your disease. This should be required reading and GI need to re-educate themselves.
Every genetic predisposition in crohn's disease, NOD2, ATG16L1, vitamin D receptors, IL-23....every single one is related to recognition of bacteria and innate and autophagy response to bacteria, every single one.
NOD2 is required for autophagy induction during AIEC infections: https://www.ncbi.nlm.nih.gov/pubmed/27335178.
When you give a crohn's disease patient an antibiotic for an unrelated infection, this could have serious consequences on their disease and the proliferation of AIEC or other bacteria, they need to know this. But if you have a GI who still thinks crohn's disease is some autoimmune disease, they don't think antibiotics affect your disease. This should be required reading and GI need to re-educate themselves.
kiny
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Regarding those L Casei probiotics. Those strains are chosen by manufacturers because they can survive in low PH, if you drink probiotics you want them to actually get to your intestine and not get killed on the way there. They have to pass the stomach before they even get to fight for their spot in the intestine.
If those L Casei inhibit AIEC, it's probably because they can survive in low PH, introducing them in the intestine will increase lactic acid and it will lower PH, it will negatively affect AIEC.
It's one thing to do this in vitro though. In the body they use biofilms, they invade macrophages, they circumvent the innate immune system on every step, they exploit autophagy defects and benefit from highly inflammatory environments, they resist most antibiotics and build up resistance very fast. Maybe some probiotics can help, but it's not enough to get rid of them.
If those L Casei inhibit AIEC, it's probably because they can survive in low PH, introducing them in the intestine will increase lactic acid and it will lower PH, it will negatively affect AIEC.
It's one thing to do this in vitro though. In the body they use biofilms, they invade macrophages, they circumvent the innate immune system on every step, they exploit autophagy defects and benefit from highly inflammatory environments, they resist most antibiotics and build up resistance very fast. Maybe some probiotics can help, but it's not enough to get rid of them.
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It's good to have you back sharing knowledge Kiny! Have you ever heard of gcMaf? It's supposed to stimulate macrophage production, in theory it could be very helpful for crohns but I don't think there have been any trials what so ever... I only know about it from a scientist, (he did map cultures for me).
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