kiny
Well-known member
- Joined
- Apr 28, 2011
- Messages
- 3,472
It seems like an odd question. By asking this you are challeging the notion of a gut mycobiome consisting of fungi.
Most studies naturally assume that when fungi like Candida spp and Malassezia are found in stool of patients with crohn's disease, that they have colonized the gut where they elicit a chronic immune response.
But there's reason to assume this is not the case. There's reason to assume these are simple transient fungal passengers that simply evoke a transient immune response.
Fungi are quite poor colonisers of the gut, due to competition from bacteria that are more flexible and can sustain higher temperatures. Most fungi are completely incapable of colonizing the gut and the diversity of species we find in stool samples are very limited, notably Candida, Saccharomyces and Malassezia.
If fungi are causing an immune response in crohn's disease, but we are not colonized by them, where then do these fungi come from. The most straightforward explanation is that they come from the diet and the oral cavity. To this day, no one has been able to explain the aphthous ulcers in the mouth of crohn's disease patients.
What is so special about EN's ability to reduce inflammation. Why is this question unanswered. When inflammatory markers drop in 24 hours, can this really be explained by a change of the microbiome? Or might it have to do with the lack of fungal antigen.
Rutgeerts and later PH Harper showed that the fecal stream elicits a strong immune response in crohn's disease, but did not suggest colonisation of the GI tract as a culprit.
Most studies naturally assume that when fungi like Candida spp and Malassezia are found in stool of patients with crohn's disease, that they have colonized the gut where they elicit a chronic immune response.
But there's reason to assume this is not the case. There's reason to assume these are simple transient fungal passengers that simply evoke a transient immune response.
Fungi are quite poor colonisers of the gut, due to competition from bacteria that are more flexible and can sustain higher temperatures. Most fungi are completely incapable of colonizing the gut and the diversity of species we find in stool samples are very limited, notably Candida, Saccharomyces and Malassezia.
If fungi are causing an immune response in crohn's disease, but we are not colonized by them, where then do these fungi come from. The most straightforward explanation is that they come from the diet and the oral cavity. To this day, no one has been able to explain the aphthous ulcers in the mouth of crohn's disease patients.
What is so special about EN's ability to reduce inflammation. Why is this question unanswered. When inflammatory markers drop in 24 hours, can this really be explained by a change of the microbiome? Or might it have to do with the lack of fungal antigen.
Rutgeerts and later PH Harper showed that the fecal stream elicits a strong immune response in crohn's disease, but did not suggest colonisation of the GI tract as a culprit.
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