Of course we all know by now that Zonulin causes these tight junctions, the barrier from the contents of the GI to the other side of the cells, to open.
It appears that in folks with celiac disease and even treated celiac disease folks that the tjs are open a lot more than normal folks. And that when exposed to gliadin that zonulin causes these tjs to open even more, a lot more in celiac disease and celiac disease-treated, but also (news to me) in folks without celiac disease. It also appears that bacteria that reside in the gut also opens these tjs (even newer news to me).
BACKGROUND AND AIMSAltered intestinal permeability is a key pathogenetic factor of idiopathic bowel inflammation. We investigated in the rat if changes in the composition of the bowel flora can alter colonic permeability.
METHODSA colonic segment was surgically excluded from faecal transit and brought out as a loop to the abdominal wall through two colostomies. The loop was used for colonisation with specific bacterial strains after eradication of the native flora with antibiotics. Lumen to blood clearance of dextran (molecular weight 70 000) and mannitol (molecular weight 182) was measured in rats recolonised with a single bacterial strain from rat colonic origin, and in control rats whose colonic loop was kept free of bacteria by antibiotics. Actual colonisation was confirmed by culture of segment effluents.
RESULTSColonisation with Escherichia coli, Klebsiella pneumoniae, and Streptococcus viridans significantly increased lumen to blood clearance of mannitol. Colonisation with Lactobacillus brevis had the opposite effect and reduced permeability to mannitol. Bacteroides fragilis did not induce significant changes. Permeability to dextran was not altered by any of the strains tested.
CONCLUSIONSCertain commensal bacteria can modify colonic wall permeability to luminal substances.
Didn't realize that even bacteria had the key to our bodies.
Here's this one that shows that zonulin was part of the key for the bacteria.
Once the tjs are open more than normal this allows stuff to pass through, in some cases gliadin and in others other food proteins or even bacteria. Once they pass through we develop the antibodies to these pathogens and all heck breaks loose.
Now I'm wondering why the gut would allow this bacteria to do this. Perhaps gliadin looks to what ever is turning on the zonulin like the bacteria and thus lets stuff on in.