Recent studies in both humans and mice suggest the immune system’s inflammatory response to fungus causes Crohn’s and colitis.
The major breakthrough came when researchers employed a different means of finding fungus in the intestinal tissue. Previously, doctors usually just looked at tissue cultures. Unfortunately, it is difficult to tease fungus out of tissue and get a culture of it. The lack of data lead mainstream doctors to believe that fungus / yeast had nothing to do with intestinal disease. Now with DNA testing, researchers have found fungus in the intestinal tissue of people with Crohn’s and Colitis.
Here is a German paper, from 2008, that says there is an increased fungal load in people with Crohn’s and Colitis.
http://www.ncbi.nlm.nih.gov/pubmed/18584522
Here is a 2012 paper by Iliyan Iliev, et al, from Cedars Sinai.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432565
These researchers showed the severity of colitis in mice depends on the way the immune system responds to fungus. Genetics that cripple the immune system’s effectiveness against fungus can cause an increased inflammatory response. They also showed that a similar gentic weakness appears to cause the same problem in humans. When they gave the mice anti-fungals, this decreased the severity of the induced colitis.
Here is a few details of the study. Colitis was induced in wild mice and in Dectin-1 deficient mice. The mice that were deficient in Dectin-1 had a more severe form of colitis. This difference in colitis severity was not due to the different bacteria present in the Dectin-1 deficient mice. The researchers implanted bacteria from the Dectin-1 mice into the wild mice and this did not change the results.
Then why would the Dectin-1 deficient mice get a more severe form of colitis? It has to do with their immune response to fungus. Without Dectin-1, the immune system has a difficult time marking the fungus for destruction. This causes the immune system to increase the inflammation. When the researchers gave the Dectin-1 deficient mice some antifungals, this reduced the severity of the colitis.
The researchers then looked at the Dectin-1 gene variations in humans. They found a halotype associated with increased severity of colitis. Humans with this halotype of the Dectin-1 gene had a much more severe form of colitis that was very difficult to treat. Hence human genetics play a big part in the severity of colitis, and this has to do with the immune system’s inability to effectively control fungus without creating a lot of inflammation.
I think this is a huge discovery. Kudos to our researchers! :thumleft:
The major breakthrough came when researchers employed a different means of finding fungus in the intestinal tissue. Previously, doctors usually just looked at tissue cultures. Unfortunately, it is difficult to tease fungus out of tissue and get a culture of it. The lack of data lead mainstream doctors to believe that fungus / yeast had nothing to do with intestinal disease. Now with DNA testing, researchers have found fungus in the intestinal tissue of people with Crohn’s and Colitis.
Here is a German paper, from 2008, that says there is an increased fungal load in people with Crohn’s and Colitis.
http://www.ncbi.nlm.nih.gov/pubmed/18584522
Here is a 2012 paper by Iliyan Iliev, et al, from Cedars Sinai.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432565
These researchers showed the severity of colitis in mice depends on the way the immune system responds to fungus. Genetics that cripple the immune system’s effectiveness against fungus can cause an increased inflammatory response. They also showed that a similar gentic weakness appears to cause the same problem in humans. When they gave the mice anti-fungals, this decreased the severity of the induced colitis.
Here is a few details of the study. Colitis was induced in wild mice and in Dectin-1 deficient mice. The mice that were deficient in Dectin-1 had a more severe form of colitis. This difference in colitis severity was not due to the different bacteria present in the Dectin-1 deficient mice. The researchers implanted bacteria from the Dectin-1 mice into the wild mice and this did not change the results.
Then why would the Dectin-1 deficient mice get a more severe form of colitis? It has to do with their immune response to fungus. Without Dectin-1, the immune system has a difficult time marking the fungus for destruction. This causes the immune system to increase the inflammation. When the researchers gave the Dectin-1 deficient mice some antifungals, this reduced the severity of the colitis.
The researchers then looked at the Dectin-1 gene variations in humans. They found a halotype associated with increased severity of colitis. Humans with this halotype of the Dectin-1 gene had a much more severe form of colitis that was very difficult to treat. Hence human genetics play a big part in the severity of colitis, and this has to do with the immune system’s inability to effectively control fungus without creating a lot of inflammation.
I think this is a huge discovery. Kudos to our researchers! :thumleft:
