there's two camps and two explanations for CD that developed over the years
-CD is caused by dysbiosis:
arguments for:
-dysbiosis can be seen
-it happens in areas where the microbiome is, ileum and colon
-people who have had antibiotics seem more susceptible to getting CD
arguments against:
-inducing colitis in mice is not relevant to the CD model in humans, it discredits a lot of microbiome studies
-the most accurate CD model is a mouse infected with an AIEC strain, not dysbiosis, however dysbiosis might enable AIEC to proliferate
-UC and CD are clinically very different diseases
-many intestinal diseases have dysbiosis, but none of them are caused by dysbiosis
-there is no consistency in the type of dysbiosis, some studies show F Prau is underrepresented, some show it is overrepresented
-the ileum is involved not because of the microbiome, but because of the peyer's patches there
-NOD2 / ATG16L1 / IL23 variants result in macrophage deficiencies, not related to the microbiome
-if only the microbiome was involved, you wouldn't expect to see transmural inflammation, nor should you see fistulas, you do in CD
-the inflammation is patchy
-fecal transplants don't seem to have a high success rate
There's also many people who are in between those arguments, AIEC is an intracellular pathogen, but you can make the crazy argument that it is part of the micriobiome, since it attaches to epithelial cells and can be found in the lumen, but most people know it is an intracellular pathogen. Just because a bacteria is found in the intestine doesn't mean you can say the cause is dysbiosis, no one says intestinal TB is caused by dysbiosis, even though there is often dysbiosis in intestinal TB, and dysbiosis makes you more susceptible to infections. Maybe some get more funding if they dress up infections as "bad and good bacteria", I don't know.
