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Crohn's Disease Forum » Books, Multimedia, Research & News » Enterome and Nestle develop FimH antagonist targeting AIEC.


05-21-2016, 05:42 PM   #1
kiny
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Enterome and Nestle develop FimH antagonist targeting AIEC.

Link:
https://www.nestlehealthscience.com/...ting-investors

20 April 2016

"Nestlé Health Science invests alongside existing investors as Enterome raises €14.5 million in Series C financing round.

Enterome will use the funds raised to advance the development of its lead drug candidate EB 8018 into first clinical studies during 2016 as a potential treatment for inflammatory bowel diseases (IBD). EB 8018 is a novel small molecule FimH antagonist licensed from Vertex that specifically targets Adherent Invasive Escherichia coli (AIEC) proliferation in the gut, one of the main causes of inflammatory colitis in IBD sufferers. AIEC is an opportunistic pathogen able to thrive in the dysbiotic gut microbiome that results as IBD develops, prolonging and exacerbating the symptoms. EB 8018 acts to restore the dysbiotic microbiome to a normal state via a novel mechanism of action whereby the adhesion of AIEC to the gut wall and its proliferation is prevented."



AIEC Video:

https://youtu.be/aTeZZ7ydmfM
05-21-2016, 05:45 PM   #2
kiny
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AIEC compiled info:

http://www.crohnsforum.com/showthread.php?t=52198
06-06-2016, 12:00 PM   #3
Scared1
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Hi Kiny,
Do you think that most of the Crohn's sufferers fall into the categories of AEIC vs. MAP based on their genetic predispositions (i.e. being able to clear one versus the other)?
06-08-2016, 02:04 AM   #4
kiny
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Hi Kiny,
Do you think that most of the Crohn's sufferers fall into the categories of AEIC vs. MAP based on their genetic predispositions (i.e. being able to clear one versus the other)?
Hm, I think people with typical crohn's disease concentrated in the ileum have symptoms that can be explained due to the proliferation of AIEC.

I don't think everyone with crohn's disease has AIEC involvement, I doubt the symptoms of people with crohn's colitis or people with little ileum involvement can be explained as easily. AIEC takes advantage of peyer's patches, that are only present in the ileum.


MAP is different I feel, because MAP requires zoonosis from farm animals or contaminated milk or water. AIEC does not, it can simply be present in the flora, familial, it can be carried by house pets like cats and dogs, it's just easier to wrap your head around, it is found far more consistently in people with crohn's disease than MAP is. If MAP is behind the inflammation, you would expect people living on farms to have far more cases of crohn's disease, that is not the case, which is a sticking point. Crohn's disease is also spreading in Asian regions, urban populations that are very lactose intolerant and consume very little dairy, how exactly are these populations coming into contact with MAP.


Genetics, no, polymorphisms in NOD2, ATG16L1 and IL-23, Vitamin D receptors would all hinder clearance of both AIEC and MAP.

Last edited by kiny; 06-08-2016 at 02:21 AM.
06-08-2016, 01:10 PM   #5
Scared1
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Hm, I think people with typical crohn's disease concentrated in the ileum have symptoms that can be explained due to the proliferation of AIEC.

I don't think everyone with crohn's disease has AIEC involvement, I doubt the symptoms of people with crohn's colitis or people with little ileum involvement can be explained as easily. AIEC takes advantage of peyer's patches, that are only present in the ileum.


MAP is different I feel, because MAP requires zoonosis from farm animals or contaminated milk or water. AIEC does not, it can simply be present in the flora, familial, it can be carried by house pets like cats and dogs, it's just easier to wrap your head around, it is found far more consistently in people with crohn's disease than MAP is. If MAP is behind the inflammation, you would expect people living on farms to have far more cases of crohn's disease, that is not the case, which is a sticking point. Crohn's disease is also spreading in Asian regions, urban populations that are very lactose intolerant and consume very little dairy, how exactly are these populations coming into contact with MAP.


Genetics, no, polymorphisms in NOD2, ATG16L1 and IL-23, Vitamin D receptors would all hinder clearance of both AIEC and MAP.
Thank you Kiny! I had read many of your other posts and really appreciate you outlining such useful information!
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