And this is a copy of a post that was made in regards to the irish times article (it explained things quite well): Original article:www.irishtimes.com/news/health/university-breakthrough-in-fight-against-crohns-disease-1.1477630
NCOT - this might offer you some insight into the immune side of things. Perhaps the immune system is for some reason unable to recognize and distinguish between good and bad bacteria and this then leads to some sort of dysbiosis that keeps popping up.... or something like that.
Reply that I liked:
This is interesting. I looked at the study abstract and since I couldn't understand it, I asked my daughter who is working on a PhD in immunology if she could explain it to me in terms that I could understand. This is her reply:
" There are a bunch of receptors on cells that recognize microbes (or sometimes even host products that signal there is an infection), these are called pattern recognition receptors (PRRs). The most famous ones are TLRs (you've probably heard me talk about
them), but the other ones are Nod-like receptors (NLRs), which includes Nod2, and mutations in this one have been linked to Crohn's disease (and since NLRs recognize microbes, that's why many people think Crohn's disease is due to not being able to recognize and respond to microbes properly).
There is a process called ubiquitination, which basically marks proteins and other products for degradation or sometimes for moving them to another
location in the cell (there are other functions, but these are the most common results). I don't know the genes/proteins they are looking at in this paper, but basically they were using mice that do not have a functional protein (Pellino3) for doing ubiquitination. They found that colitis in these mice was worse, and they also checked in CD patients and found they had lower levels of Pellino3.
Then they looked to see what this protein actually does, and it is responsible for adding ubiquitin to RIP2. If Pellino3 isn't around, then RIP2 isn't ubiquinated, and this meant that there was less NF-kB and MAPK activation (these are major pathways that respond to microbial infection and also are responsible for creating lots of inflammatory products). This is interesting, because most people want to reduce inflammation in CD, but this study seems to indicate that less inflammation (because NF-kB and MAPKs weren't as activated) actually made the disease worse. There are lots of functions of NF-kB and the MAPKs beside just creating inflammation, but it's still really interesting (which is probably why this is in Nature Immunology, arguably the best immunology journal). "
Diagnosed Crohns-Colitis about
8 years ago - Past Meds: Antibiotics, Prednisone, Methotrexate, Remicade - Current Meds: No meds at the moment -Trying Amino Acid Balancing Therapy Actually achieved full clinical remission for about
2 years using Remicade, Diet (SCD) and Exercise
“The only person you're destined to become, is the person you decide to be"... wise words