# World Slowly Awakens to Role of Inflammatogenic Mechanisms in IBS



## Mike NoLomotil (Jun 6, 2000)

Gut 2002 Jul;51 Suppl 1:I41-I44 A Role for Inflammation in Irritable Bowel Syndrome?Barbara G, De Giorgio R, Stanghellini V, Cremon C, Corinaldesi R.Department of Internal Medicine and Gastroenterology, University of Bologna, Bologna, Italy.Attention has been directed to the putative role of low grade mucosal inflammation in irritable bowel syndrome (IBS) on the basis of evidence showing that some patients with IBS have an increased number of inflammatory cells in the colonic and ileal mucosa. Previous episodes of infectious enteritis, genetic factors, undiagnosed food allergies, and changes in bacterial microflora may all play a role in promoting and perpetuating this low grade inflammatory process. Human and animal studies support the concept that inflammation may perturb gastrointestinal reflexes and activate the visceral sensory system even when the inflammatory response is minimal and confined to the mucosa. Thus abnormal neuroimmune interactions may contribute to the altered gastrointestinal physiology and hypersensitivity that underlies IBS. A brief review of the human and animal studies that have focused on the putative role of intestinal inflammation and infections in the pathogenesis of IBS is given.PMID: 12077063 [PubMed - in process] ________________Old news becomes new when the right people see it.


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## ohnometo (Sep 20, 2001)




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## eric (Jul 8, 1999)

FYI" Jack Wood, PhD Professor of Physiology and Internal Medicine Chairman Emeritus, Department of Physiology The Ohio State University College of Medicine Dr. Wood was the first to use microelectrodes to record the electrical and synaptic behavior of neurons in the enteric nervous system. He coined the term "brain-in-the-gut" in view of emerging evidence that the enteric nervous system had neurophysiological properties like the brain and spinal cord. In recent years he has focused on signaling interactions between the enteric immune system and the brain-in-the-gut during infectious enteritis and food allergy. In this lecture he shows how the central nervous system, enteric nervous system and intestinal immune system are integrated during physical and emotional stress to produce irritable bowel symptoms of diarrhea and abdominal pain and discomfort. "" Esther Sternberg, MD Chief, Section on Neuroendocrine Immunology and Behavior Director, Molecular, Cellular and Behavioral Integrative Neuroscience Program National Institute of Mental Health, National Institute of Health A pioneer in the field of neural-immune interactions, Dr. Sternberg will present the scientific evidence proving molecular, neuroanatomical and hormonal links between the brain and immune system and will discuss the role that disruptions of such links play in inflammatory/autoimmune disease. ""Nigel Bunnett, PhD University of California School of Medicine Department of Surgery and Physiology Accumulating evidence indicates that sensory nerves play a major role in inflammation of multiple tissues, and that communication between the nervous system and mast cells is of particular importance. Dr. Bunnettï¿½s lecture will highlight recent experimental evidence that mast cell proteases signal to sensory nerves through novel receptors that couple to the release of proinflammatory peptides, and that defects in this mechanism result in uncontrolled inflammation and disease. Dr. Bunnett will present evidence that therapies designed to block signaling by neuropeptides and proteases are attractive treatments for inflammation. " http://www.conference-cast.com/ibs/Lecture...dRegLecture.cfm


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## eric (Jul 8, 1999)

FYIPost infectious IBS"Low-grade inflammatory changes may persist in some of these patients. " http://www.med.unc.edu/medicine/fgidc/post_infestious.htm


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## Mike NoLomotil (Jun 6, 2000)

More Old news posted as "new news", and posted as if it is refutory to something, which in fact it is not, it is complementary. This is the reatest weakness in assessment of Irritable Bowel Syndrome patients still...failure to take a complementary view.The piont is that simply because one shows that the origin of an inflammtory response may be other than the innate inflammatogenic systems themselves does not remove the primary innate inflammatogenic systems from consideration.Quite the opposite it EXPANDS the understanding, and expands the view that in the simpest terms possible it is a 2-way, 3-way, even 4-way street, as illustrated best by Zar et al. if one takes the time and effort and objectivity to study the diagram set forth in that tutorial. All that is missing is the circulating immunocyte reactions confirmed by Bengtsson et al...which can be added byd rawing a line to mediator release from non-IgE mechanisms.To achive maximum effectiveness, maximal therapeutic response, one must now consider that either a top-down model of inflammtogenic response or a bottom-up model may be primary, and the other secondary, as far as primary insult goes in a given patient. Since it can be both ways one must approach the problem that way.There is no value, for example, to attemptimg to suggest that the "discovery" of "t cell" responses in the small bowel of IBS victims which can be provoked by direct instillation of specific foods is a primary top-down phenomenon when there is ample direct evidence to suggest that it is local mechanism. In fact it is merely a possibility whivh is worthy of further investigation, as is a primary aberrant immunologic response to which the CNS aberrations observed may be secondary.Fortunately effective therapy for IBS patients does not have to wait for science to finish the chicken-or-egg debate (since insufficient evidence exists to establish if there even is a chicken-egg issue to be dabated). At some point someone will integrate the two perspectives on the reserch, the two methodologies (jejunal isolation and observation vs. top-down studies of CNS activity). It is being considered, a wellr espected site has offered to perform the research, and funding for same needs to be accumlated.At least, since science now knows that what was alleged in 1956 to be a problem repsonsoble for these symptoms is true, once can proceed with effective disease managment protocols which integrate top-down therapies AND bottom-up therapies, if one seeks to do so, and ensure the best outcomes for their patients.This is a great leap forward from just a year ago when the dogma was loudly trumpeted here and in some other quarters that "there is no inflammation in IBS", and those who suggested that there was such a process involved were labelled quacks and charlatans and at best fools. Now the exact people struggle to somehow establish that "they were on this all along".


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