Hi Ginny,
Hmmmm. You do know how to ask a good, thorny question, don't you. LOL. OK, here are my thoughts on this issue:
While Dr. Symes chose to call his article,
What is the “Leaky Gut”?, he didn't discuss the details of the mechanism by which The Leaky Gut Syndrome, (LGS), actually allows oversize and "forbidden" objects to leak into the bloodstream. Instead, he chose to focus on the agents which, in his opinion, cause the destruction of the villi of the small intestine. While it is certainly true that destruction of the villi is somewhat closely linked with LGS, technically, they are separate events, and one event doesn't necessarily guarantee that the other event will be a result, (though there are obviously indirect connections, depending on the types of immune system responses which occur).
I could be wrong, but IMO, LGS must be present before the villi begin to develop atropia. In reality, of course, the two events almost certainly occur somewhat simultaneously, over a relatively long period of time, but it is probably necessary for LGS to allow a sufficient number of pathogens, or allergens, to pass through the tight junctions, before damage to the enterocytes comprising the mucosal surface, can begin, since most of the damage to the enterocytes is initiated from below, (in the submucosal region), by killer T-cells, and intraepithelial lymphocytes.
The critical connection, though, is the fact that as the enterocytes are damaged/destroyed, the local tight junctions are obviously going to fail, and the integrity of the entire mucosal surface will soon be in dire jeopardy, resulting in an accelerated failure rate, as more and more junctions open, allowing more and more "forbidden" items to escape into the bloodstream.
The most unique aspect of his description of the issue, of course, is the observation that it is the glutenous nature of the respective prolamin proteins in the offending foods, that is key to the destructive results of the process. I don't recall seeing it described that way, by any other authority. Certainly, the excellent article by Dr. Fasano, that appeared in the August, 2009 issue of Scientific American, never mentioned than an agglutinating effect was involved in the process.
http://somvweb.som.umaryland.edu/absolu ... 8.2009.pdf
So is DogtorJ right? As I said, I wouldn't argue against him, because what he says is certainly logical. All of the offending prolamin proteins that contain the peptides to which gluten-sensitive individuals react, are certainly agglutinating agents, and the peptides involved are lectins, to boot. Nor are any weak spots apparent in his description. If scientific proof of this theory has been published, I certainly haven't seen it, but that doesn't mean that it doesn't exist, nor does it mean that scientific proof will not be forthcoming, at some point in the future.
From a macroscopic viewpoint - if such a glutenous mass were to glom onto the surface of the mucosa, and refuse to let go, it is easy to visualize a smothering effect, that could result in a desperate attempt by the immune system to break it up, in the only way it has available - by killing the mucosal cells, (the enterocytes), that the mass is attached to, so that the whole mess will float away.
That's my 2 cents worth, FWIW.
Tex