What do you mean by "many animals are functionally lacking a microbiome, and many have transient microbiomes"?I don't think this has any diagnostic value. Any number of infections can cause luminal content to enter tissue.
But it does show how easy luminal content enters tissue, and how permeable the intestinal barrier is.
A recent Nature study from march showed that around 14 percent of patients who had given blood samples for routine hospital controls had luminal content of bacterial origin in the blood sample. Undetected by regular tests.
It would be interesting to see these studies in animals too. It is often assumed that animals naturally have microbiomes, due to the sheer amount of studies coming out. But this is untrue, many animals are functionally lacking a microbiome, and many have transient microbiomes. The percieved benefits for humans is vastly overstated too. Large reductions in bacterial load with dietary intervention like EN, do not result in nutritional defficiencies, but instead drastically lower inflammatory markers in crohn's disease.
A gut microbiome is usually lauded for its benefits to the host, rarely is the cost for the host dicussed.What do you mean by "many animals are functionally lacking a microbiome, and many have transient microbiomes"?
Thanks! This makes me wonder if a diet that is diverse should be considered a modern day phenomenon and is helping all kinds of old and new bacteria thriving in the gut which might not be beneficial like what we think it is?A gut microbiome is usually lauded for its benefits to the host, rarely is the cost for the host dicussed.
The cost to the host is that a microbiome competes with the host for nutrients and becomes pathogenic when commensal bacteria or fungi cross the epithelial barrier.
The benefit/cost analysis is poor for many animals, so they either completely lack a microbiome, or have transient microbiomes where bacterial load is very low. Many bird species, panda species, host only small or transient microbiomes.
This is likely a result of evolution and diet, where the microbiome became a risk factor in their survival.
There is a cost to humans too. Crohn's disease doesn't develop where there aren't any bacteria, crohn's disease develops in the ileum, colon and mouth where the bacteria and fungi reside.
When bacteria and fungi cross the epithelial barrier in crohn's disease, immune cell in the lamina propria set off an immune response and you get deep transmural inflammation. But if one drastically changes the diet with EN, it deprives the microbiome of nutrients which lowers bacterial load, and lowers the cost we pay for hosting a microbiome.
How do they diagnose gastritis when it's inactive?Btw I think what Kiny says makes a lot of sense, but I recently found this study that basically says chronic inactive gastritis is almost universal in Crohns patients: https://www.nature.com/articles/s41598-022-21630-5
They also noticed a curious phenomenon, about h pylori being much less prevalent in Crohns patients vs controls. But the most curious thing about this is the location being the stomach. Btw I had upper endoscopy 1.5 years before my Crohns diagnosis which came back with the same exact findings, although deemed of questionable clinical relevance.
Any other microorganism that could potentially turn harmful when the opportunity presents itself?Commensals and probiotics are often described as these low-harm bacterial species without invasive properties.
In a healthy individual with a competent GI barrier these bacteria are kept at bay, the mucus layer is in tact, the epithelial barrier is sealed off between cells with proteins called tight junctions. The barrier lets through nutrients and little else.
In people with crohn's disease who have active inflammation, this is all compromised, likely due to pathogenic bacteria and fungu who enter tissue and set off the immune cells in the lamina propria.
Suddenly those "low-harm" commensals become pathognic (they become "pathobionts" if you wish), they enter tissue through mechanical force, through the fecal stream, and they are no longer harmless.
There's a mouth-gut axis, where species like klebsiella and veillonella that normally reside in the mouth, likely end up in the intestine. These are ingested with saliva. In normal people these would simply be washed away with the fecal stream, in people with active inflammation, these would enter tissue.Any other microorganism that could potentially turn harmful when the opportunity presents itself?
They did a biopsy on a healthy / normal looking stomach (I also didn't have any symptoms resembling gastritis as far as I could tell, neither did others in the study I linked), and that's when they saw it. There are specific chronic signs histopathologists look for that are distinct from active ones - as far as I understand the presence of neutrophils causing ongoing inflammation distinguishes active from inactive gastritis, while infiltration of lymphocytes in the lamina propria is seen in both.How do they diagnose gastritis when it's inactive?