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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over the past several years, a number of studies have addressed the role of specific strains of bacteria, or combinations thereof, to alleviate certain symptoms of irritable bowel syndrome (IBS). More importantly, the precise factors that contribute to this therapeutic effect, such as modulations in cytokine levels and alterations in colonic motility, are being clarified. This review serves to summarize the evidence for the use of probiotics in the treatment of IBS and to place this information in clinical context. Potential future developments and areas of possible research are also discussed.
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PMID:Probiotic use in irritable bowel syndrome. 1683 44

Over the past two decades, our understanding of interleukin-16 (IL-16) has increased substantially. Initial studies characterizing IL-16 as a chemotactic cytokine (but not a chemokine) just scratched the surface of the unique properties of this cytokine. Since then, scientists have determined that IL-16 has a wide range of effects on cells, including upregulation of CD25, induction of cells to progress to the G(1) phase, inhibition of antigen- specific proliferation yet with retained antigen nonspecific proliferative properties, and discovery of a novel neuronal form with unique properties. Recently, a plethora of studies have implicated IL-16 in exacerbation of infectious, immune-mediated, and autoimmune inflammatory disorders, including atopic dermatitis, irritable bowel syndrome, systemic lupus erythematosus, neurodegenerative disorders, and viral infections. Herein, we review the body of evidence supporting a role for IL-16 in infectious and immune-mediated inflammatory disorders and explore the known and possible mechanism of actions in the numerous diseases.
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PMID:Not-so-sweet sixteen: the role of IL-16 in infectious and immune-mediated inflammatory diseases. 1688 62

Irritable bowel syndrome (IBS) is a functional disorder which affects the 20% of the population. The exact origin is unknown. IBS is the result of interaction of genes and environmental factors. Familial aggregation and higher concordance rate of monozygotic twins compared to dizygotic twins provide evidence for the importance of genetic factors in the pathogenesis of IBS. Interest has focused on genetic variants of serotonin transporter and receptors, because of their role in gut motility, visceral sensitivity, immune processes and mood. Firm conclusions about the role of serotonin system, as well as other neuroreceptors, G-proteins, cytokine polymorphisms in the pathogenesis of IBS cannot be made.
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PMID:[Genetic background of irritable bowel syndrome]. 1689 32

Irritable bowel syndrome may be consisted of several subsets of functional disorders including a subset of post inflammatory and post infectious disorders. Animal models revealed prolonged hyper-kinesis of the intestinal muscle and visceral hyperalgesia in adult mice previously received phychological stress or bowel irritation in neonatal period. Murine infectious experiment reproduced adult post infectious functional disorders. Involvement of acute phase Th2 cytokine production and prolonged TGFbeta1 production contribute to intestinal hyper-kinesis in post nematode infectious rat model. Pathogenesis of irritable bowel syndrome may be further subdivided by the results of experimental models, and a novel therapeutic approach is expected from such experimental models.
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PMID:[Post infectious irritable bowel syndrome experimental model]. 1689 8

The CD40-CD154 pathway is important in the pathogenesis of inflammatory bowel disease. Here we show that injection of an agonistic CD40 mAb to T and B cell-deficient mice was sufficient to induce a pathogenic systemic and intestinal innate inflammatory response that was functionally dependent on tumor necrosis factor-alpha and interferon-gamma as well as interleukin-12 p40 and interleukin-23 p40 secretion. CD40-induced colitis, but not wasting disease or serum proinflammatory cytokine production, depended on interleukin-23 p19 secretion, whereas interleukin-12 p35 secretion controlled wasting disease and serum cytokine production but not mucosal immunopathology. Intestinal inflammation was associated with IL-23 (p19) mRNA-producing intestinal dendritic cells and IL-17A mRNA within the intestine. Our experiments identified IL-23 as an effector cytokine within the innate intestinal immune system. The differential role of IL-23 in local but not systemic inflammation suggests that it may make a more specific target for the treatment of IBD.
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PMID:Differential activity of IL-12 and IL-23 in mucosal and systemic innate immune pathology. 1692 Jun 36

In the present study we have characterized T cell-driven immune function in mice that are genetically deficient in PKC theta. In response to simple immunologic stimulation invoked by in vivo T cell receptor (TCR) cross-linking, these mice showed significantly depressed plasma cytokine levels for IL-2, IL-4, IFNgamma, and TNFalpha compared to wild-type (WT) mice. In parallel, spleen mRNA levels for these cytokines were reduced, and NF-kappaB activation was also reduced in PKC theta knockouts (KO). Injection of allogeneic cells into the footpad of PKC theta deficient mice provoked a significantly diminished local T cell response compared to WT mice similarly challenged. Unlike comparable cells from wild type mice, CD45RBhi T cells harvested from PKC theta deficient mice failed to induce colitis in the SCID-CD45RB cell transfer model of IBD. In another T cell-dependent model of inflammatory disease, PKC theta deficient animals developed far less severe neurologic signs and reduced spinal cord inflammatory cell infiltrate compared to WT controls in the MOG-induced EAE model. A fundamental role for PKC theta in T cell activation and in the development of T cell-mediated inflammatory diseases is indicated by these results.
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PMID:Mice deficient in PKC theta demonstrate impaired in vivo T cell activation and protection from T cell-mediated inflammatory diseases. 1706 26

Infection by pathogenic organisms leads to mucosal damage and disruption of the gut's extensive commensal flora, factors which may lead to prolonged bowel dysfunction. Six to 17% of unselected irritable bowel syndrome (IBS) patients believe their symptoms began with an infection, which is supported by prospective studies showing a 4%-31% incidence of postinfectious IBS-(PI) following bacterial gastroenteritis. The wide range of incidence can be accounted for by differences in risk factors, which include in order of magnitude; severity of initial illness > bacterial toxigenicity > hypochondriasis, depression and neuroticism, and adverse life events in the previous 3 months. PI-IBS has been reported after Campylobacter, Salmonella, and Shigella infections. Serial biopsies after Campylobacter jejuni gastroenteritis show an initial inflammatory infiltrate, with an increase in enterochromaffin (EC) cells, which in most cases subsides over the next 6 months. Those who go on to develop IBS show increased numbers of EC and lymphocyte cell counts at 3 months compared with those who do not develop IBS. Interleukin-1beta mRNA levels are increased in the mucosa of those who develop PI-IBS, who also show increased gut permeability. Recover can be slow, with approximately 50% still having symptoms at 5 years. Recent studies suggest an increase in peripheral blood mononuclear cell cytokine production in unselected IBS, an abnormality that may be ameliorated by probiotic treatment. The role of small-bowel bacterial overgrowth in IBS is controversial, but broad-spectrum antibiotics do have a temporary benefit in some patients. More acceptable long-term treatments altering gut flora are awaited with interest.
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PMID:Role of infection in irritable bowel syndrome. 1723 25

Postinfectious irritable bowel syndrome (IBS) is a subgroup of IBS. Patients with an episode of bacterial gastroenteritis may have a 12-fold increased risk of developing IBS symptoms within the same year. The IBS can be manifested in each of its clinical types, but the diarrhea-predominant form occurs most commonly. The primary pathophysiologic factor in developing IBS after enteral infection may be defects in enteric nervous system which can produce abnormality in visceral hypersensitivity and intestinal motility. These patients also display exaggerated increases in mucosal immunocompetent T lymphocytes and an abnormally high pro- versus anti-inflammatory cytokine ratio, providing evidence to the contribution of the immune system in the development of postinfectious IBS. Via bi-directional brain-gut interactions both peripheral and central events can play a role in the development of clinical symptoms. Stress is associated with significant worsening of the complaints in IBS and may also result in a shift in the host-gut microbial relationship. IBS itself may predispose patients to acute bacterial gastroenteritis because of the altered intestinal motility. It needs further clarifying the relationship between IBS and small intestinal bacterial overgrowth syndrome. Upon the data so far the altered intestinal flora in IBS would merely reflect developments due to altered motility and not a causal relationship. The treatment of postinfectious IBS does not differ principally from that of the idiopathic IBS. Antibiotics or probiotics may lead to temporary symptomatic improvement, but, given the lack of evidence based data, they cannot be advised for routine use so far.
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PMID:[Postinfectious irritable bowel syndrome]. 1729 54

The mammalian intestinal epithelium is a unique model for studying cellular differentiation since it undergoes continuous and rapid renewal. Substantial new information has accumulated on the mechanisms of regulation of the gene expression (e.g. Wnt, Hedgehog, bone morphogenic proteins), and the cell proliferation and apoptosis of the intestine. New knowledge has been gained in areas of genetics, central nervous system and enteric nervous system neurotransmitters (e.g. serotonin, corticotrophin-releasing factor, endogenous cannabinoid system, pathogen associated molecular patterns) of motility, sensitivity and secretion, the effect of altered mucosal inflammation on cytokine and paracrine activation, and neural sensitization, postinfectious disorders, the influence of psychologic stress on gut functioning through alterations in regulatory pathways, and improved accuracy of diagnosis both at the gut and brain level. In addition, acknowledgement of these mechanisms might help to develop strategies for therapy of neuronal abnormalities, which cause different gastrointestinal disease (e.g. irritable bowel syndrome, Crohn's disease). The present review focuses on the relationships between the gene expression and the intestine, and furthermore, presents the evidence and gastrointestinal diseases of the autonomic nervous system, the humoral factors, and the immune functions related intestinal proliferation and apoptosis.
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PMID:Relationships between the autonomic nervous system, humoral factors and immune functions in the intestine. 1735 22

High-mobility group box 1 (HMGB1) is a nuclear factor released extracellularly as a proinflammatory cytokine. We measured the HMGB1 concentration in the sera of mice with chemically induced colitis (DSS; dextran sulfate sodium salt) and found a marked increase. Inhibition of HMGB1 by neutralizing anti-HMGB1 antibody resulted in reduced inflammation in DSS-treated colons. In macrophages, HMGB1 induces several proinflammatory cytokines, such as IL-6, which are regulated by NF-kappaB activation. Two putative sources of HMGB1 were explored: in one, bacterial factors induce HMGB1 secretion from macrophages and in the other, necrotic epithelial cells directly release HMGB1. LPS induced a small amount of HMGB1 in macrophages, but macrophages incubated with supernatant prepared from necrotic cells and containing large amounts of HMGB1 activated NF-kappaB and induced IL-6. Using the colitis-associated cancer model, we demonstrated that neutralizing anti-HMGB1 antibody decreases tumor incidence and size. These observations suggest that HMGB1 is a potentially useful target for IBD treatment and the prevention of colitis-associated cancer.
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PMID:Essential roles of high-mobility group box 1 in the development of murine colitis and colitis-associated cancer. 1759 6


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