# IBS, infection and inflammation



## Jackie (Sep 15, 2004)

Medline article: IBS - A Postinfectious and Inflammatory Disorder? Nicholas J. Talley, MD, PhD Digestive Disease Week 2000 Day 3 - May 23, 2000 ...The article headings are:Can Infection Change Gut Sensory Perception?Is There Evidence of Increased Inflammation in IBS? Post-Campylobacter Enteritis and IBSThe article concludes that "The results of these new studies are exciting. There appears to be increasing evidence that IBS and probably other functional gastrointestinal disorders are, at least in a subset, due to structural disease. Host and bacterial factors may both be important. The development of new disease markers appears likely from the novel work in progress. This in turn should lead to characterization of more homogenous groups of patients and the development of better-targeted therapeutic approaches (perhaps NK-1 antagonists). Clinicians should watch this space!" http://www.medscape.com/medscape/cno/2000/...m?story_id=1296 (to view this article it may be necessary to join Medscape)Jackie http://bara.idx.com.au/dfragilis/links.htm


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## Mike NoLomotil (Jun 6, 2000)

COMMENT:This is an interesting question posed:"Is There Evidence of Increased Inflammation in IBS? "The first published evidence the involvement of immunologic ("inflammatory") mediators involved in IBS dates all the way back to 1980 in my files. Throughout the 1980s and 1990s it has been seen many times in studies which quantify specific mediators or which measure symptoms against treatment outcomes with drugs which reduce or block immunologic response in the gut.In the referenced article I am surprised (literally) that Dr. Tornbloom is not working with Dr. Bengsston...at least they do not appear to be....they should...at least they are in the same country doing similar jejunal investigations!Better give each other the phone number.Also, the subpopulation of 1 in 4 may be post-infective etiology would not be inconsistent with epidemiologic studies....several investigators have found that the inflammatory rmediators found in the referenced studies do not require preinfection or other trauma as a precursor events to be present.As I have posted before, the competion of the picture should occur over the next 3-4 years as more people start looking into the small bowel microvasuclature, mucosa, lamina propria, and neural structure.MNL______________ www.leapallergy.com


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## eric (Jul 8, 1999)

Some more on all this. This came out a while ago and is clues to the begingings of IBS for some. The thing here is that the inflammation is gone and your left with IBS.DR Wood is a top researcher.ScienceIrritable bowel symptoms may herald inflammatory enteric neuropathyBy Karla GaleWESTPORT, Jul 13 (Reuters Health) - Patients who initially present with symptoms of irritablebowel syndrome may develop chronic pseudo-obstruction, apparently mediated by autoimmuneattack on the enteric nervous system, according to Dr. Jackie D. Wood of Ohio State University,in Columbus."What we have seen in patients with pseudo-obstruction is that about 5 to 10 years before, theywere experiencing abdominal pain, and alternating between diarrhea and constipation," Dr.Wood told Reuters Health. "But there would be no obvious biochemical or structuralabnormality to account for it." "These patients should be tested for autoimmune neuropathy," he continued. "If one can identify itearly in its course and if it can be reversed with anti-inflammatory drugs or corticosteroids, thenwe may save people from a disastrous life later on."In the June issue of the European Journal of Gastroenterology & Hepatology, Dr. Wooddescribes the results of enteric neuropathic degeneration. Self-excitable smooth muscle, in theabsence of inhibitory motor neurons, spread contractions in the uncontrolled syncytium that"collide randomly." Propulsive motility subsequently fails.Pseudo-obstruction related to inflammatory neuropathies includes paraneoplastic syndrome,Chagas' disease and idiopathic degenerative disease, according to the paper. Double-labelimmunohistochemistry testing of a patient's serum can demonstrate the presence of entericneuronal antibodies.Dr. Wood predicted that tests for circulating factors similar to those in rheumatoid arthritis orlupus will be developed. If the presence of circulating antibodies in a patient's serum is confirmed, he told Reuters Health,the next step would be a full-thickness biopsy. "If the histology showed an inflammatory attackon neurons, that is when the clinician would start aggressive therapy," he concluded. Eur J Gastroenterol Hepatol 2000;12:597-600.-Westport Newsroom 203 319 2700A newer study:Am J Physiol Gastrointest Liver Physiol 2001 Mar;280(3):G315-G318 Related Articles, Books, LinkOut Stress and the Gastrointestinal Tract IV. Modulation of intestinal inflammation by stress: basic mechanisms and clinical relevance. Collins SM McMaster University Medical Centre, Hamilton, Ontario L8N 3Z5, Canada. [Record supplied by publisher] The stress response in a healthy organism is generally viewed as a warning and thus a protective reaction to a threat. However, the response may be deleterious if it is linked to an inflammatory stimulus or if it proceeds an inflammatory event. Prior stress enhances the response to an inflammatory stimulus by a mechanism that is independent of the release of hypothalamic corticotropin-releasing factor (CRF) or arginine vasopressin. Putative mechanisms include an increase in intestinal permeability as well as the release of the proinflammatory neuropeptide substance P. Stress may also reactivate previous inflammation when applied in conjunction with a small luminal stimulus. This reactivation involves increased permeability and requires the presence of T lymphocytes. Inflammatory mediators activate hypothalamic pathways, and a negative feedback loop, mediated by CRF release, has been proposed because animals with impaired hypothalamic CRF responses are more susceptible to inflammatory stimuli. Together, these experimental observations provide insights into the expression of inflammatory disorders in humans, including inflammatory bowel disease and postinfective irritable bowel syndrome. PMID: 11171612 ------------------I work with Mike and the audio 100 program. www.ibshealth.com www.ibsaudioprogram.com


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## Mike NoLomotil (Jun 6, 2000)

This is a nice tidy summary of the primary functional aspexts of the main mediators when elicited within the bowel in response to whatever stimulus should trigger the tissue response and the granulocyte repsonse within the GIT:--------------------------------------------1: Can J Gastroenterol 1999 Mar;13 Suppl A:42A-46aEFFECTS OF INFLAMATORY MEDIATORS ON GUT SENSITIVITYBueno L, Fioramonti J Department of Pharmacology, INRA, Toulouse, France. lbueno###toulouse.inra.frOver the past decade, attention has been paid to the role of visceral sensitivity in the pathophysiology of functional bowel disorders, especially irritable bowel syndrome, and visceral hypersensitivity is the most widely accepted mechanism responsible for both motor alterations and abdominal pain. Inflammatory mediators sensitize primary afferents, especially C-fibre polymodal nociceptors, favouring the recruitment of silent nociceptors that give rise to secondary spinal sensitization. After local tissue injury, the release of chemical mediators such as potassium ions, ATP, bradykinin and prostaglandin E2 directly activate nerve endings and indirectly trigger the release of algesic mediators such as histamine, 5-hydroxytryptamine and nerve growth factor from other cells, which, in turn, stimulate proximal afferent nerve endings and silent nociceptors. Among the intermediary structures activated by inflammatory mediators and susceptible to the release of proalgesic substances, mast cells and platelets play a crucial role; however, immunocytes such as macrophages and neutrophils or sympathetic nerve terminals are also candidates. Moreover, events likely to activate synthesis of mediators by mast cells, such as stress and septic shock, also trigger colonic hypersensitivity. Prolonged visceral hyperalgesia may also depend on spinal sensitization. A number of substances are candidates to play a role at the spinal cord level in mediating painful and nonpainful sensations. Among them, substance P, dynorphins and glutamate play a pivotal role in postsynaptic sensitization, particularly during and after gut inflammation. Finally, despite the complexity of the relationship between inflammatory mediators and gut hypersensitivity, numerous results strongly suggest that alteration in neuroimmune communications at the gut level may trigger a series of events that give rise to chronic changes in visceral sensitivity.


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