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Crohn's Disease Forum » Books, Multimedia, Research & News » Caltech ATG16L1 T-Reg Discovery


05-08-2016, 11:06 AM   #1
xeridea
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Caltech ATG16L1 T-Reg Discovery

Caltech researchers have discovered that a mutation related to the ATG16L1 gene may prevent the body from throwing the "Off" switch. So rather than commensal bacteria activating an immune response, this is saying that beneficial bacteria cannot turn off the immune response.

The researchers found that if just one of these two genes was absent, the mice were unable to develop disease-protective immune cells called regulatory T cells in response to B. fragilis—and that even after treatment with B. fragilis, symptoms in an ATG16L1-deficient mouse model of intestinal disease remained unchanged.
05-08-2016, 11:23 AM   #2
Scared1
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I thought this was anninteresting article - except it said in some cases this maybbe the cause. I wish people can just test for these genes and say yes or no - you have crohn's. And i was hoping the article would say why the suddenr onset happens at different stages in life even though people have these genes unchanged their entire life.
05-09-2016, 11:14 AM   #3
xeridea
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I thought this was anninteresting article - except it said in some cases this maybbe the cause. I wish people can just test for these genes and say yes or no - you have crohn's.
Yes, it's frustrating that research can't just come out and give all the answers. From my layman's perspective, it seems Crohn's is a spectrum of diseases with too many factors contributing to it. Also, the immune system varies so much among individuals, so maybe really hard to design trials that can take all the variables into account.

And i was hoping the article would say why the sudden onset happens at different stages in life even though people have these genes unchanged their entire life.
Maybe it's not really sudden but something gradual that eventually reaches a tipping point. Perhaps at each exposure a little more B/T memory cells are produced and each successive exposure evokes a stronger reaction.
05-09-2016, 12:58 PM   #4
wildbill_52280
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This part is what has the most significance in my opinion. Humans not rats.

Chu and Mazmanian then obtained blood samples from both healthy patients and patients with Crohn's disease at the Cedars-Sinai Medical Center in Los Angeles. "We could see that certain patients' immune cells responded to Bacteroides fragilis, while immune cells from other patients didn't respond at all," Chu says. "Because the cells from Cedars had already been genotyped, we were able to match up our results with the patients' genotypes: immune cells from individuals with the protective version of ATG16L1 responded to the treatment, but cells from patients who had the mutated version of the gene showed no anti-inflammatory response to B. fragilis." - See more at: https://www.caltech.edu/news/when-be....zQ94iJJr.dpuf
Yet I wonder how certain their conclusions really are and what this may mean for the promise of restoring the microbiome with Fecal Microbiota Transplants. Rarely do I stumble across good evidence against the theory of microbiome restoration but I'm afraid to admit this kind of suggests Fecal transplant benefits may be limited. Many studies on nod2 though already exist and is pretty inconclusive in regards to connection to crohn's lots of people carry the gene and never develop crohn's, so this study probably doesn't give the whole story either. There is still plenty of hope for microbiome restoration with Fecal transplants. I recall there are some personal differences to the type of bacteria which someone responds to, so its like donor and patient may someday need to be tested for microbiome compatability to better predict FMT success. here is a paper recently released on the subject http://caelushealth.com/wp-content/u...i_20160429.pdf

This also reminds me of the one report of a woman possibly cured of crohn's with FMT which was a patient of Dr. Borodys in australia, they used 3 donors at the same time. This would likely provide a wide variety of organisms which would increase the compatability with the patient/host. It was also performed using a nasogastric tube, for all these reasons this may explain why she was one of the few crohn's patient that achieved rapid and long lasting success supposedly 13 year "remission" verified with a colonoscopy. So with this study from caltech, the species and strain just may not be compatible with the host and limit any broad conclusions to be derived from it. It would be interesting if other strains were tested that might still be able to stimulate these cells in a situation where b.frag would not be able to, so rather stimulate the cells "despite" the atg mutation.
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Last edited by wildbill_52280; 05-09-2016 at 01:16 PM.
05-10-2016, 08:22 AM   #5
Scared1
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I do agree - there is much more to this whole fecal transplant/gut bacteria situation.

On a separate note - do you guys think that give the state of news these days - the clear interplay between gut bacteria and someone's immune system, that ALL patients with Crohn's must have the genetic mutation? Are there patients they can test that do NOT have this mutation yet have Crohn's?
05-19-2016, 09:05 PM   #6
irishgal
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If anyone is interested, I posted this article in our site's private Facebook group about a week ago and John Aitken gave an off the cuff commentary on it! Interesting read if you want to join the group:
https://www.facebook.com/groups/1558...?ref=bookmarks
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Past (failed) Treatments: Remicade, Humira, Prednisone, Pentasa, Azulfadine, Lialda, No gluten/dairy/sugar/coffee or processed food in general. Flagyl worked but not long term.
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