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Intestinal fungal commensals and food-derived yeasts, drives inflammatory CD4+ T cell responses in patients with CD
- Thread starter kiny
- Start date
kiny
Well-known member
For what it's worth. Most of the weird immune terms being used and the implication of diet mentioned in the study.
T helper cells, or CD4+ T cells, and their subgroups, Th1, Th2, and recently the newly discovered third subset and was named Th17. The cytokine Th17 releases is interleukin 17. Note that IL-17 blockade failed in crohn's disease trials. When CD4+ T cells notice microbes in the intestine, these 3 subgroups, Th1, Th2 and Th17 proliferate.
Another term is interferon Y, or IFN-Y, or interferon gamma, all the same thing. It's easy to remember, the reason it's called interferon...is because it interferes with viral infection. IFN-Y is a macrophage activator. These macrophages, which the intestine has extremely high concentration of, cause phagocytosis of microbes. Your innate immune response to fungi and bacteria is the physical mucus layer, the epithelial cells, anti-microbial peptides, and activation of macrophages and dendritic cells in the tissue below, or lamina propria.
Anyway, this ASCA test that is often used to differentiate CD from UC, tests for antibodies against the carbohydrate cell wall of S. cerevisiae. About 60 percent of people with CD are ASCA+, meaning they react to baker's yeast, or there is some cross reactivity going on. The relevance of this has been questioned a lot, because healthy people consume bread and other nutrients with this yeast all the time without issues, but this is a solid study showing people with CD with ASCA+, react to this yeast. If you are ASCA+, and your medical records should be able to show this, it is probably advised to limit these fibers to limit the exposure of immune cells to S. cerevisiae.
T helper cells, or CD4+ T cells, and their subgroups, Th1, Th2, and recently the newly discovered third subset and was named Th17. The cytokine Th17 releases is interleukin 17. Note that IL-17 blockade failed in crohn's disease trials. When CD4+ T cells notice microbes in the intestine, these 3 subgroups, Th1, Th2 and Th17 proliferate.
Another term is interferon Y, or IFN-Y, or interferon gamma, all the same thing. It's easy to remember, the reason it's called interferon...is because it interferes with viral infection. IFN-Y is a macrophage activator. These macrophages, which the intestine has extremely high concentration of, cause phagocytosis of microbes. Your innate immune response to fungi and bacteria is the physical mucus layer, the epithelial cells, anti-microbial peptides, and activation of macrophages and dendritic cells in the tissue below, or lamina propria.
Anyway, this ASCA test that is often used to differentiate CD from UC, tests for antibodies against the carbohydrate cell wall of S. cerevisiae. About 60 percent of people with CD are ASCA+, meaning they react to baker's yeast, or there is some cross reactivity going on. The relevance of this has been questioned a lot, because healthy people consume bread and other nutrients with this yeast all the time without issues, but this is a solid study showing people with CD with ASCA+, react to this yeast. If you are ASCA+, and your medical records should be able to show this, it is probably advised to limit these fibers to limit the exposure of immune cells to S. cerevisiae.
kiny
Well-known member
If they're correct and the fungi are coming from oral sources, then it's important to wrinse your mouth with water after you drank EN. Not because there's fungi in EN, there's obviously not, but becausing just leaving EN in the mouth is just a sure way to fuel candida, you also don't want EN to touch your teeth. Avoiding dietary yeast is not difficult, it's found in products using leavening agents like batter, pastry and bread, and it's in a handful of dairy products.
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What would be your latest update Kiny? as regards to research and breakthroughs and new medications as a summary.
How is the crohns world progressing do you think?
We do have new meds there has been more research, are you noting anything that is pointing in any direction more clearly with the science, and any new meds to support this?
I guess also that not all known info is available for everyone yet from labs or pharma companies either.
How is the crohns world progressing do you think?
We do have new meds there has been more research, are you noting anything that is pointing in any direction more clearly with the science, and any new meds to support this?
I guess also that not all known info is available for everyone yet from labs or pharma companies either.
kiny
Well-known member
We're not very good dealing with stenosis and fistula. Crohn's disease is a penetrating disease for many. A lot of young kids with crohn's disease tend to now have an aggressive disease course, including penetrating disease, meaning they develop lots of fistulas early on. No organ is more capable of renewing itself than the intestine. But deregulated wound healing results in stenosis or fistula. A lot of researchers are looking at how this process actually occurs in the intetine and how fibroblasts are activated and which growth factors are involved in it. Closing internal fistula and reversing stenosis is a goal for much of the research. It should be possible to stimulate closure of fistula for examply by activating fibroblasts.
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