The thing that will be interesting in studying IBSACOL will indeed be which element of the small bowel immune dysfunction is affected. All the sodium cromoglycate studies done so far have demonsrated mucopsal mast cell involvement in part, even in non-atopic patients. This was s surprise until The Swedes started finding the mixed circulating cell and mast cell responses of the small bowel mucosa in direct in vivo jejunal isolation studies over the last 4-5 years. Apparent humoral response but absent specific characerictics of humoral immune respnse. Things that make ya go Hmmmmmm....The mechansisms of the response of the granulocytic cells in the microvascualature is actually easier to to understand, (cellular immunity repsonse) esp. when a recent study of the lamina propria using full thicknes biopsy of small bowel found clear evidence of the involvement of the compement mechansism (alternative pathway), but in the words of Brostoff, the mucosal response is King...ie...primary yet there is no specific IgE to the provoking foods seen yet...just what the response is, what the mediators are, and markers for the reactions and of course what these chemicals do in the gut ans syetmically once they are released is well known so when these reactions are seen it is not hard to udnerstand where the symptoms and altered neural function come from.By the by, this comment drew my interest: ----------------"...I have heard from those who did that Dr. Meakin repeatedly referred to "inflammation in IBS" - to the derision of those members present, who appear to know rather more about IBS than he does...." ----------------If someone was foolish enough to deride Dr. Meakin for referring to "inflammation in IBS" and to label themselves as someone who "knows rather more than he does about IBS" I would suggest a reading of the Talmud: -----------------"If silence be good for the wise, how much better for fools" -----------------The dogma of "no inflammtion in IBS " is about 5 years out of date. I the first place the statement is as meaningless as saying "there is no water in a desert". There is. You just ain't lookin in the right place so you are doomed to never see it. That does not make the claim true, not being able to sdiscern it. And you may even be thinking of water in the wrong context as well.The fact that no "inflammatory response" has been seen in the colon has been the source of the "conventional wisdom", and itself is now conventional folly since full thickness biopsies of the ileocecal junction show increase mast cell density in SOME IBS victims. End of word NO.This is one of the first markers that was seen that suggested that the shock organ is not the large bowel but the small bowel. The recruitment of increased numbers of mast cells to the cecum in these patients suggests a site oc chronic insult at the point the small bowel empties into the large bowel.Further, in vivo and in vitro findings have for at least the last five years showing the shock organ and site of the abnormal immunologic response to be the small intestine, where food and additives are first presented to the humoral and cellular immune system elements...and that they are reacting with aberrant "inflammatory" reactions. When the mediators of inflammatory response are present, "no inflammation" becomes a untrue. Done. This is the first "chemical step" in either a umoral or cellular response...dumping peformed mediators and synthesis of others.The release hitamine, seroroninf and of an array of leukotrienes, cytokines, synthesis of prostaglandins, complement-sensitizition and numerous other markers are "inflammatory markers".If "members present" DERIDE Dr. Meakin for making a factual statement they merely are reflecting their own ignorance of the physiology. I am sorry that I was not present at the time If Dr. Meakin was "derided" for making accurate statements.As was also pointed out in this thread, the presupposed mechanism may or may not be correct and I for one would also like to assess the mechansism, and do know what tools need to be accessed to assess that mechanism. But there is no basis for "more knowledgaeble members [deriding] Dr. Meakin" for expressing a fact, unpopular as that fact may be with some people in and out of some elements the medical community and patient community.Now the terms "overt inflammation" described as absent, esp. if applied to the colon, is a much more accurate use of verbiage, as "inflammatory response" and the different types of cellular infiltration, interraction, tissue responses, and cellular consequences can and are distinctive. So if one is looking for localized eosinophilic infiltrate in the colon, for example, one will come away disappointed unless one seeks to show "no inflammation". If one is looking for lymphocyte aggregation, inflamatory mediators present, loss of cell wall integrity in granulocytes, altered vascular permability, etc. in the small bowel structures one will come away with those inflammatory markersd and events in hand from challenges of the jejunum in confirmed reactive patients (oral challenge confirmed prior to jejunal challenge with subsequent in vivo and in vitro analysis of markers).I hope no one representing this Community embarrassed themselves by "deriding Dr. Meakin", especially if they feel proud of themselves for it.Eat Well. Think Well. Be Well.MNL_______________
www.leapallergy.com [This message has been edited by Mike NoLomotil (edited 03-20-2001).]