Most studies of UC are based on DSS colitis models and so that's where we can mostly draw information from. Unfortunately, these studies hardly get at most of the questions you listed. Those models are only really good at studying how inflammation occurs in the absence of a mucus barrier and how our immune system reacts to gut bacteria. It might be an accurate model if erosion of the mucus barrier is how UC is initiated, but if its not, then the DSS models only address a small aspect of how the disease is generated.
I can't speak for anyone else, but one of my new favorite hobbies is coming to this forum just to bounce ideas back and forth with other members on what might be going on. I like talking science, and it hones my skills as someone who eventually wants to get into research and/or medicine. I don't think anyone here is expecting to actually solve the disease, but I feel like the time I spend thinking about
the disease anyway is more constructive in discussions I have with others here.
For example, an idea I had in another thread about
if researchers have studied the differences between healthy and diseased colonic tissue in UC in humans that don't have pancolitis is something I might bring up with my doctor, who follows UC research. Perhaps our murmurs can get a discussion going in research circles and one day they might start a study for that. It would be really interesting to see how some of our tissues stay healthy while the same tissue is diseased elsewhere. I also think asking the question of why UC always starts distally is an important question if we want to figure out pathogenesis.
At present, I think it's a strong motivation for researchers to learn more about
IBD because the disease is still really unpredictable in most people. Like AZYooper said, I wouldn't care so much about
having UC if we were able to have good, stable control over it. It's the constant unpredictability and uncertainty that makes it a challenge to live with, presently.
EDIT: I also find the geographical distribution of IBD interesting. From that data, they say that exposure to sunlight may have an effect on if you get the disease or not. But sunlight's immunosuppressive effects go beyond just helping you produce vitamin D, although that helps too.
The bit about
germ-free mice is also really interesting too, because that seems to be a pretty strong indication that the immune attack is against our gut bacteria, rather than our colon autoantigens. Seems like no one is really thinking that the immune attack is actually against our colons, these days, and it is much more likely against our gut bacteria.
Post Edited (Tunnelvisionary) : 10/16/2014 2:58:42 PM (GMT-6)