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Although this doesn't mention IBS it is how stress stress and inflammation"Neurogenic Inflammation in Chronic Pain Conditions "We usually associate inflammation with the response of the body to tissue injury or invasion by hostile microorganisms. The central and autonomic nervous systems play an essential role in the initiation and modulation of this process. Although tissue trauma or infectious agents may be initiating factors in neurogenic inflammation, neither of them are required. The inflammation may be initiated and maintained by the central and peripheral nervous systems in response to psychological stress[1]" http://216.109.125.130/search/cache?p=hpa+...&icp=1&.intl=usYou here about "Macroscopic inflammation" in IBS.It is believed the mast cells in the gut are effected by stressors in IBS and they degrandulate from stressors without a pathogen.They then release histimine onto the smooth muscles of the gut (toxic), which can contribute to pain in IBS along with the problems they already see in the serotonin system in IBS.

 

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Inflammatory Changes Seen in Irritable Bowel Chronic Pelvic PainA DGReview of :"Neurogenic inflammation and chronic pelvic pain"World Journal of Urologyhttp://www.docguide.com/news/content.nsf/n...ritable%2CbowelLecture: Neurophysiology of Brain-Gut Interactions During Stress Presenter: Jack Wood, PhD "Jack Wood, PhDProfessor of Physiology and Internal MedicineChairman Emeritus, Department of PhysiologyThe 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. "http://www.conference-cast.com/ibs/Lecture...cfm?LectureID=7"Irritable bowel syndrome (IBS) is a functional intestinal disorder characterised by changes in bowel habits, which range from constipation to diarrhoea, associated with abdominal discomfort or overt pain (Drossman et al., 2002; Talley & Spiller, 2002). These symptoms can be attributed to modifications of the sensory-motor function of the intestine, where the substrate(s) involved could reside within the intestinal wall, in extrinsic ganglia, or in the central nervous system (Camilleri, 2001). As has recently been pointed out (Drossman et al., 2003), psychological distress, affective disorders, and narcotic abuse have to be considered as important ethiopathogenetic factors for IBS; however, there is little doubt that such factors also trigger peripheral changes. In accordance with this concept, stress can reactivate a previous peripheral inflammation (Collins, 2001), thus establishing a link between psychological factors and post-infectious (or post-dysenteric) IBS (Spiller et al., 2000). Current pharmacological treatments are aimed at controlling specific symptoms (e.g., tricyclic antidepressants for pain, 5-HT3 antagonists or spasmolytics for diarrhoea, 5-HT4 agonists for constipation) and the improvement obtained is relatively modest (Mertz, 2003). Therefore, a single drug that could potentially affect all of these symptoms would represent an important therapeutic achievement (Kirkup et al., 2001)."http://www.nature.com/bjp/journal/v141/n8/full/0705751a.html

 

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Critical role of mast cells in inflammatory diseases and the effect of acute stress"AbstractMast cells are not only necessary for allergic reactions, but recent findings indicate that they are also involved in a variety of neuroinflammatory diseases, especially those worsened by stress. In these cases, mast cells appear to be activated through their Fc receptors by immunoglobulins other than IgE, as well as by anaphylatoxins, neuropeptides and cytokines to secrete mediators selectively without overtdegranulation. These facts can help us better understand a variety of sterile inflammatory conditions, such as multiple sclerosis (MS),migraines, inflammatory arthritis, atopic dermatitis, coronary inflammation, interstitial cystitis and irritable bowel syndrome, in which mast cells are activated without allergic degranulation."http://216.109.125.130/search/cache?p=mast...&icp=1&.intl=us

 

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"Neurobiology of Stress and InflammationPsychological, environmental, or physical stress activatesthe hypothalamic-pituitary-adrenal axis (HPA axis) andthe sympathetic nervous system. Inflammatory stimuliat the periphery will also activate the HPA axis.(Developmentally, inflammatory response is the moreprimitive surveillance system and it precedes establishmentof the nervous system). All of these stimuli will activatethe HPA axis in a similar way, leading to increased outputof major stress hormones (e.g. corticosteroids,catecholamines, growth hormone and others) and theinitiation of an acute phase response (APS) resulting inthe inflammatory process.Peripheral Nerves and Inflammatory ProcessThe autonomic and somatic nerve fibers are closelyassociated with inflammatory cells, including mast cells.Many of them are identifiable as substance P (SP)containing C fibers. In addition to SP, these fibers releaseother neuropeptides involved in the inflammatory process(calcitonin gene related peptide [CGRP], neurokinin Aand B, somatostatin and others.) The close physicalrelationship between the C fibers and mast cells is ofparticular importance, as SP released from the nervefibers degranulates mast cells. During degranulation, the mast cells release multitudes of proinflammatory agents.These agents include: nerve growth factor (NGF), tumornecrosis factor-á (TNF-á), histamine, heparin, proteases,interleukins, serotonin and others. Such a release inducesan inflammatory response in the form of vasodilatation(redness) and plasma protein extravasation (edema).Additionally, newly released nerve growth factor (NGF)stimulates a further increase in the number of neuronalfibers, thus increasing the potential for further releases of SP and the transmission of nociceptive impulses."http://66.218.69.11/search/cache?p=Neuroge...&icp=1&.intl=us