The paper said this specifically on page four
IBD paper said...
"Although many species were highly coated (ICI > 10) in both IBD and control groups, 35 species were uniquely highly coated in patients with IBD"
I believe that means those 35 species were only coated in the patients with IBD.
Almost done with the paper, but a major point I read seems to be that when the highly coated IgA bacteria were introduced into germ-free mice, no immediate reaction happened, however in mice with DSS induced colitis, those highly coated species of bacteria induced a much more severe form of the disease.
Even though I'm not finished with the paper, to me, this indicates that perhaps the initial cause of the immune reaction may not be because of the bacteria, but the makeup of your gut bacterial community may GREATLY influence the severity of your disease. That's still a really good thing to know, imo. What this leaves is what causes that initial immune response?
EDIT:
This part sticks out to me too
Somebody said...
Because most innate immune receptors involved in the detection of bacterial pathogens sense microbial components present in both pathogens and commensals (e.g., lipo-polysaccharide), the mechanisms by which the immune system distinguishes between pathogens and commensals remain largely unknown. However, one way the immune system is thought to distinguish between pathogens and commensals is by sensing pathogen-associated activities or behaviors, such as adherence to the intestinal epithelium, tissue invasion or destruction, or the ability to colonize normally sterile mucosal environments, such as intestinal crypts
Perhaps... an initial break in the mucus barrier allows the bacteria to go where they shouldn't be and the immune system marks them for destruction because it resembles what pathogenic bacteria do, even though these are normally harmless bacteria. The more highly IgA coated species you have in your gut, the more severe your disease, the more your mucus barrier breaks down because your immune response is much stronger.
Hmm...anyone have thoughts on this?
EDIT 2: The researchers seem to conclude the same sort of thing as I wrote above. I now see why OM dismissed a bacterial CAUSE. But this paper seems to strongly support the idea that your microbiome makeup highly influences the severity of disease. It also suggests that the bacteria responsible may be highly individual, which would explain why probiotics, fecal transplants, and antibiotics work great for some and horribly for others.
After flagyl, I noticed that I started having slightly more pain and cramping afterwards, and my stools are also less formed in general. But I was having bloody stools for 4-5 months without any of those features after my initial course of antibiotics which induced the UC. Perhaps the alteration of my gut bacteria from flagyl is responsible for the change, though I can think of other things that might influence this.
Post Edited (Tunnelvisionary) : 8/28/2014 9:17:54 PM (GMT-6)