Can the hyphae form invade the tight junctions of the intestinal tract or is it too large? I had someone from another message board tell me that it was too large to actually invade the tight junctions itself, but cellular bits and pieces could basically hold them open. I think that the TJs are inappropriately chemically opened at wrong times and the candida wouldn't necessarily have to push it's way through. I've been unable to find any studies about this. Anyone know of any biopsies, etc. that actually showed this?
Candida may be larger than the tight junctions (I have no idea if it is or not), but that doesn't mean it couldnt still fit through there. I've seen what small plant roots can do to concrete, so it doesn't seem all that impossible to me.
Thanks!
Shonda
Candida question
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Hi Shonda,
Whoever told you that is mistaken. I have mentioned that candida can penetrate the tight junctions between epithelial cells, numerous times on this board, thus contributing to the leaky gut syndrome, but I don't believe that I've ever referenced any research to substantiate that claim. Here is pretty clear proof of that phenomenon. This research was conducted on a rabbit tongue, but all epithelial tissue is similar, and all epithelial tissue in the GI tract is especially similar:
The red emphasis is mine, of course. Note that the article mentions that the growth pattern resembles thigmotropism.
In this particular situation, clearly, the term refers to candida growing "around" the cells, and therefore, into, and through, the tight junctions.
The fact that candida albicans filaments might be larger that the tight junctions is irrelevant, since the tight junctions are normally closed, which implies integral contact between cells. Therefore, by definition, the filaments would have to be larger than the "gap", when a gap is not even present. The peptides that pass through the tight junctions to cause LGS symptoms, are obviously larger than the "normal" gap in the tight junctions, also. Once the tight junctions open, all bets are off. Your example of roots growing through cracks in concrete or rock, is a perfect example of why the initial size of the tight junctions is irrelevant.
There are a lot of references listed below the abstract that I cited, many of which contain addition insight into this phenomenon. Such as:
http://www.ncbi.nlm.nih.gov/pubmed/7747 ... t=Abstract
Note this observation, from the abstract below, (again, the red emphasis is mine):
This one describes the examination of human biopsy specimens from white patches on the mucosae of tongue and lips, by means of conventional electron microscopy techniques:
http://www.ncbi.nlm.nih.gov/pubmed/811778?dopt=Abstract
You're most welcome,
Tex
Whoever told you that is mistaken. I have mentioned that candida can penetrate the tight junctions between epithelial cells, numerous times on this board, thus contributing to the leaky gut syndrome, but I don't believe that I've ever referenced any research to substantiate that claim. Here is pretty clear proof of that phenomenon. This research was conducted on a rabbit tongue, but all epithelial tissue is similar, and all epithelial tissue in the GI tract is especially similar:
http://www.springerlink.com/content/l584u71274435804/C. albicans produced characteristic hallmarks of pathological tissue invasion in both tissue models over a period of 48 h. Hyphae penetrated through epithelial cells and intercellular gaps latter resembling thigmotropism.
The red emphasis is mine, of course. Note that the article mentions that the growth pattern resembles thigmotropism.
http://en.wikipedia.org/wiki/ThigmotropismThigmotropism is a movement in which an organism moves or grows in response to touch or contact stimuli. The prefix thigmo- comes from the Greek for "touch". Usually thigmotropism occurs when plants grow around a surface, such as a wall, pot, or trellis.
In this particular situation, clearly, the term refers to candida growing "around" the cells, and therefore, into, and through, the tight junctions.
The fact that candida albicans filaments might be larger that the tight junctions is irrelevant, since the tight junctions are normally closed, which implies integral contact between cells. Therefore, by definition, the filaments would have to be larger than the "gap", when a gap is not even present. The peptides that pass through the tight junctions to cause LGS symptoms, are obviously larger than the "normal" gap in the tight junctions, also. Once the tight junctions open, all bets are off. Your example of roots growing through cracks in concrete or rock, is a perfect example of why the initial size of the tight junctions is irrelevant.
There are a lot of references listed below the abstract that I cited, many of which contain addition insight into this phenomenon. Such as:
http://www.ncbi.nlm.nih.gov/pubmed/7747 ... t=Abstract
Note this observation, from the abstract below, (again, the red emphasis is mine):
http://www.ncbi.nlm.nih.gov/pubmed/1575 ... t=AbstractHyphal penetration into the superficial epithelium, particularly at cell junctions, together with features of cellular internalization of yeasts was noted. Phospholipase activity was visible at the tips of hyphae and initial sites of bud formation. Further, SEM studies revealed cavitations on the surface epithelial cells particularly pronounced at the sites of hyphal invasion. Hyphal invasion was seen both at cell surfaces and intercellular cell junctions of the epithelium, the latter resembling thigmotropic behaviour.
This one describes the examination of human biopsy specimens from white patches on the mucosae of tongue and lips, by means of conventional electron microscopy techniques:
http://www.ncbi.nlm.nih.gov/pubmed/811778?dopt=Abstract
You're most welcome,
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.