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The increased production of the antibacterial enzyme lysozyme in CC and LC supports a bacterial aetiology for these two diseases. Lysozyme upregulation in different cell types (epithelial vs macrophages) supports the notion that CC and LC might be two different maladies.
Lamina propria T lymphocytes seem to have lost their physiological unresponsiveness to several microbial antigens. All these observations suggest that Crohn's disease may be caused by hyperreaction of the local cellular immune system to numerous microbial and nutritional antigens normally present in the intestine.
Maybe, but that's not exactly overwhelming evidence. The presence of the enzyme obviously verifies that it is associated with the disease, and it introduces the possibility of a bacterial connection, but it doesn't necessarily provide a strong case for a bacterial etiology. That enzyme is present in many body excretions, such as saliva, tears, human milk, mucus, etc. Large amounts can be found in egg white, and that's where it was first discovered, (it's antibacterial properties led to the discovery of penicillin). The researcher who discovered penicillin, determined that snot, (or more politely - mucus from a patient with a head cold), had antibacterial attributes when applied to bacterial cultures.The increased production of the antibacterial enzyme lysozyme in CC and LC supports a bacterial aetiology for these two diseases.
Since the laboratory markers of LC and CC are quite different, (lymphocytic infiltration of the mucosa, versus collagen band thickening in the lamina propria) , it's not surprising that LC might show "Marked lysozyme immune-reactivity in subepithelial lamina propria mucosa (lpm) macrophages", whereas CC showed "marked lysozyme expression in the colonic crypts". Until/unless lysozyme is accepted as a required marker for diagnosis of the disease, such distinctions are of academic interest, only.Lysozyme upregulation in different cell types (epithelial vs macrophages) supports the notion that CC and LC might be two different maladies.
(I'm inclined to believe that it does, of course.) At any rate, that's certainly an interesting discovery.
Once again, I'm contemplating the nuclear option of a course of antibiotics plus anti-fungals, followed by probiotics and a grain-free diet. All my autimmune issues started during a post-partum period marked by a bladder infection and 4 rounds of mastitis and LOTS of antibiotics. Could this be the trigger and not the pregnancy at all? I'm tired of wondering and waiting. I need answers!!over-consuming corn, as so many Celiac patients do since they have few other choices of grains in their diet, is likely to propagate the illness. Many people have successfully treated (dare we say cured?) their Celiac disease by not only avoiding grains altogether--especially corn--but also including antifungal medications in their treatment regimen. Such antifungals may include the natural, coconut-derived fatty acid known as Caprylic acid (available over the counter), or stronger, prescriptive antifungals.
The net result has probably resulted in our immune system becoming overwhelmed with issues that it was never evolved to handle. Our immune system evolved on whole food, not "designer" food.I don't recall the exact numbers, but research shows that approximately half of all celiacs are not 100% faithful to the diet, either due to occasional or frequent cheating, or because of failing to be diligent enough in label-reading, etc., or from accidental exposure due to cross-contamination, or incorrect labeling, (which happens far more often than most people realize). That makes them all vulnerable to developing other autoimmune issues, including MC. In many cases, I'll bet the damage was already done before they were initially diagnosed with celiac disease, because of the poor diagnostic rate. In some cases, both diseases are diagnosed at the same time, and in others, it probably takes a while before the additional food sensitivities became "mature". Many doctors stop looking, once they find either celiac disease, or MC, so the other disease isn't discovered until later, when a patient fails to respond to treatment. That's probably especially true when celiac disease is diagnosed first.Zizzle wrote:And why are celiac patients developing MC despite strict adherence to the GF diet? Something else must be at play here...
Most mycotoxins develop in the fields, while the grain is growing, or while it is maturing, but in some cases, it can also become worse, during storage, if storage conditions are not correct, (IOW, if grains is stored with too much moisture, the problem can increase). Yes, immature corn is safe, (aflatoxin, for example, cannot develop until the grain dries down to below roughly 18% moisture). Fresh corn, (roasting ears), should have a moisture level at least up in the 40 to 50% range, so it is perfectly safe. I'm not aware of any mycotoxins that commonly infect rice. Corn, grain sorghum, (milo), wheat, (and related grains, such as barley and rye, spelt, etc.) are vulnerable, both in the field, and in storage. (Wheat doesn't normally develop aflatoxin, or fumonison, but it can develop vomitoxin, zearalenone, etc., if growing conditions are unusually moist).Zizzle wrote:If we want to avoid these mycotoxins, are they primarily found in stored grains? Is fresh corn OK? Does rice harbor the same levels of fungi?
The first food item in which aflatoxin was discovered, is peanuts, (a legume), and aflatoxin is still a problem with peanuts. Hopefully, the regulators do a decent job of minimizing the risk, but I'm pretty sure that a fair number of contaminated peanuts reach market, because they're uniquely vulnerable to fungal growth, due to the fact that moisture control is more difficult while they are still in the shell, (they're harvested in the shell, and usually stored that way, until final disposition). (Never eat a moldy-looking peanut.) Cotton is not a legume, but cottonseed is another food product that often has a serious aflatoxin problem. It's claimed that the oil should be safe, but we all know how shaky a similar claim about soy protein not existing in soy oil, turns out to be, for anyone with MC.Zizzle wrote:Is any grain safe? Do dry beans and legumes also carry fungi?
I'm back to simply stating an opinion, here, again, but IMO, the multiple doses of antibiotics are probably much more likely to have caused long-term autoimmune problems, and gut bacteria population issues, than the hormonal changes that occur with pregnancy.Zizzle wrote:All my autimmune issues started during a post-partum period marked by a bladder infection and 4 rounds of mastitis and LOTS of antibiotics. Could this be the trigger and not the pregnancy at all?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1433141/In the present study sera from coeliac disease patients from the United Kingdom and the United States were assayed for neutralising antibody to Ad12 as evidence of past exposure to that virus and for antibody to synthetic peptides of A-gliadin from the region of shared sequence with the Ad12 E1b protein. Eighty nine per cent of untreated coeliac disease patients had evidence of previous Ad12 infection.
"CD" stands for "celiac disease", of course, and TLRs stands for toll-like receptors.In the 1980s a 12-amino acid sequence homology was found between A-gliadin and the E16 protein from the human adenovirus type 12 (16). More recently epidemiological observations on the seasonal pattern of incidence of CD have sustained the hypothesis of a viral infection triggering the disease (17). Rotavirus, as seems obvious from the articles by Stene et al and Zanoni et al, is a good candidate.
The scenario that can be envisioned is that the contact with gluten at a time when there is ongoing intestinal inflammation, altered intestinal permeability, and type I and type II interferon production, upregulation of HLA-DQ2 and HLA-DQ8 on dendritic cells, will increase the risk for developing CD, at least in a subset of individuals. At the same time, the phenomenon of molecular mimicry may trigger autoimmunity. The possibility that these antibodies, among their other biological activities, may modulate the innate immune response through activation of TLRs, is a new, intriguing observation.
The part that I've emphasized in red, defines why molecular mimicry is possible. If you're asking why we would react to the alpha gliadin peptide, that's because it mimics a similar peptide in the amino acid chain that defines rotovirus. By coincidence, those two amino acid sequences are identical, except for a single amino acid position. That's known as molecular mimicry.Innate cellular immunity recognizes viral infection using toll-like receptors (TLRs), or pattern recognition receptors, which sense Pathogen-associated molecular patterns (PAMPs), triggering the expression of nonspecific antiviral proteins.
Maybe, because the innate immune system does not respond differently upon repeat infection by the same pathogen - it continues to provide the same old response - (it never learns any better).Joe wrote:Is this an issue of a 'tipping point' given the constant presence of gluten the 'standard diet' producing a persistent response by the immune system.
