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Query: UMLS:C0009319 (colitis)
 19,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolonged antigenic stimulation results in lymphocyte shedding of CD27, a member of the tumour necrosis factor receptor (TNFR) family, and transformation to a stable phenotype capable of synthesizing interleukin-4 (IL-4). Co-expression of alpha4beta7 identifies those cells with gut-homing potential. We have investigated these cell populations in patients with inflammatory colonic disease. Circulating and lamina propria mononuclear cells were isolated from patients with Crohn's disease (CD), ulcerative colitis (UC), non-inflammatory bowel disease (non-IBD) colonic inflammation and healthy controls. Double and triple colour flow cytometry for CD3, CD4, CD27, alpha4beta7 and intracellular cytokines was performed. Circulating CD4+ CD27- populations were increased in patients with CD (8.8 +/- 0.8%, P < 0.001), UC (12.2 +/- 1.9%, P < 0.001) and non-IBD colitis (10.5 +/- 1.3%, P < 0.01) as compared with controls (6.1 +/- 0.5%). CD4+ CD27- alpha4beta7+ cells were increased in CD (P < 0.01). Lamina propria CD4+ CD27- populations were depressed significantly in CD (P < 0.05), UC (P < 0.02) and non-IBD colitis (P < 0.03). Mucosal CD4+ CD27- cells synthesized IL-4 in preference to interferon-gamma. Thus, colonic inflammation is associated with alterations in gut-tropic circulating and mucosal populations of differentiated memory T cells with the phenotype of predominantly IL-4-synthesizing cells.
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PMID:Variation in gut-homing CD27-negative lymphocytes in inflammatory colon disease. 974 20

Large intestinal disease, and more especially colitis, is a commonly seen problem in small animal practice. Although colitis is most frequently diagnosed in dogs, it is becoming increasing common in cats. The etiology of colitis is not known, but there is general agreement that an immune-mediated response to luminal antigen is involved. In particular, parasites, bacteria and dietary factors may be involved. In approximately 10% of dogs presented with typical signs of colitis, no pathologic lesion will be found on investigation. These dogs have a functional diarrhea associated with some stress factor and are thought to have irritable bowel syndrome (IBS). This condition is most frequently observed in working dogs, although highly nervous and excitable dogs may also exhibit similar clinical signs. Until the underlying etiology of colitis is determined, treatment regimens will remain symptomatic. Recent studies have placed considerable importance on the value of diet in the prevention, immediate and long-term therapy of colitis in dogs and cats. In particular the value of "novel" protein diets, fermentable fiber and polyunsaturated fatty acids is receiving the most attention. It is now possible to maintain patients in long-term remission and to modify the severity and chronicity of colitis by using diet alone. This paper will review the subject of dietary management of colitis and IBS and present results from the author's clinical research program.
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PMID:Diet and large intestinal disease in dogs and cats. 986 50

In this review, I hope to have highlighted that cytokines are of crucial importance in the normal homeostasis of the gut immune system, the interactions of the gut immune system with enteric antigens and also in tissue injury associated with IBD. There is evidence from a number of different systems that the response to nominal non-replicating antigens, administered nasally or orally, is skewed towards a non-Th1 type of response. To say that the response is Th2, Th3 or Tr is premature. IL-10 and TGF beta seem to be important in downregulating potentially tissue-damaging Th1 responses to the normal flora and possibly food antigens. However, it need to be seen whether the mouse results also apply to humans. A consistent pattern in disease states, whether it be human or mouse, is an exaggerated Th1 type response with excess local production of IFN-gamma and TNF alpha, and its association with tissue injury. An important question to address is whether this represents a switch from the Th2, Th3, or Tr pathway towards a Th1 pathway, or whether the Th1 pathway is in fact always present in the gut, but is kept in check and non-pathogenic by regulatory cells. Equally important is the need to discover where regulation occurs: is it in the PP or the lamina propria? Intriguing results from Kronenberg and colleagues have shown that SCID mice reconstituted with CD45RBhi or CD45RBlo cells show no difference in the re-population of the gut prior to disease (ARANDA et al. 1997). The reason for colitis developing in those mice reconstituted with CD45RBhi cells is therefore more complex than merely differential re-population kinetics. No matter what the outcome is, these and other related questions dealing with the induction and expression of mucosal T-cell responses are going to produce some surprises in the next few years.
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PMID:Effector and regulatory lymphoid cells and cytokines in mucosal sites. 989 58

Morphometry was carried out of the surface epithelium, of crypts as a whole and their epithelium in rectal mucosa (RM) biopsy specimens from patients with irritable colon syndrome (ICS) and chronic non-infectious unspecified colitis (ChNUC). Of the RM morphometric parameters, it is the intestinal crypt external diameter (CED) that exhibited most extensive correlations, which fact enabled the authors to use CED for systematization of ICS and ChNUC patients. Interrelationship was established between CED, ICS clinical picture and ChNUC rates.
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PMID:[The mucosal status of the large intestine in the irritable bowel syndrome and in chronic noninfectious nonspecific colitis]. 1005 Apr 76

Several authors have described an association between celiac disease (CD) and ulcerative colitis (UC), but this has not yet been established. The aim of our study was to examine the frequency of antigliadin antibodies (AGA), antireticulin antibodies (ARA) and antiendomysium (AEM) antibodies in the sera of patients with UC (n = 50), and to evaluate their correlation with clinical variables. Sixteen patients with irritable bowel syndrome (IBS) and 37 healthy individuals served as controls. An enzyme-linked immunosorbent assay was used for the detection of IgA- and IgG-type AGA. IgG-type ARA were determined by an indirect immunofluorescence assay (IIF) using rat kidney, liver, and stomach as antigen substrates. IgA-type AEM antibodies were measured by IIF, using cryostat sections from human umbilical cord. Seventeen of the 50 patients with UC (34%) were positive for IgA- or/and IgG-type AGA. There was no correlation between the presence of AGA and the duration or extent of the disease, or disease activity. However, 5 patients with both IgA- and IgG-types of AGA had extensive colitis. Only 2 controls (4%) were positive for IgG-AGA. ARA and AEM were not detected in any individuals studied. Since the ARA and AEM test results were negative, we conclude that none of the UC patients in this series had CD.
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PMID:High frequency of antigliadin antibodies and absence of antireticulin and antiendomysium antibodies in patients with ulcerative colitis. 1020 12

In the present study we investigated the possible therapeutic effects of bombesin on an experimentally induced colitis model in rats. Inflammation of the colon was induced by a single intracolonic administration of 30 mg of 2,4,6-trinitrobenzene sulfonic acid (TNBS) at 8 cm from the anus. Immediately after the induction of colitis, some rats were given bombesin (10 microg/kg; subcutaneously) three times a day for 14 days, while another group received vehicle treatment. On day 14, the rats were decapitated and plasma carbonyl content and tissue myeloperoxidase level, as an index of granulocyte infiltration into intestinal tissue, were determined in order to obtain an objective evaluation of colonic injury. In the colitis group, increased macroscopic damage score, elevated MPO level and high plasma carbonyl content, together with the microscopic appearance revealed severe inflammatory changes resembling IBD. Bombesin treatment attenuated the TNBS-induced colonic damage and stimulated histopathologically apparent mucosal proliferation, suggesting that bombesin may play a role in protecting gut integrity.
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PMID:Bombesin ameliorates colonic damage in experimental colitis. 1049 29

Inflammation of the intestine causes pain and altered motility, at least in part through effects on the enteric nervous system. While these changes may be reversed with healing, permanent damage may contribute to inflammatory bowel disease (IBD) and post-enteritis irritable bowel syndrome. Since little information exists, we induced colitis in male Sprague-Dawley rats with dinitrobenzene sulfonic acid and used immunocytochemistry to examine the number and distribution of enteric neurons at times up to 35 days later. Inflammation caused significant neuronal loss in the inflamed region by 24 hours, with only 49% of neurons remaining by days 4 to 6 and thereafter, when inflammation had subsided. Eosinophils were found within the myenteric plexus at only at the earliest time points, despite a general infiltration of neutrophils into the muscle wall. While the number of myenteric ganglia remained constant, there was significant decrease in the number of ganglia in the submucosal plexus. Despite reduced neuronal number and hyperplasia of smooth muscle, the density of axons among the smooth muscle cells remained unchanged during and after inflammation. Intracolonic application of the topical steroid budesonide caused a dose-dependent prevention of neuronal loss, suggesting that evaluation of anti-inflammatory therapy in inflammatory bowel disease should include quantitative assessment of neural components.
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PMID:Damage to the enteric nervous system in experimental colitis. 1051 87

Segmental colitis which showed the similar findings of ulcerative colitis and right-sided colitis with back-wash ileitis has been considered as the unusual form of ulcerative colitis. Today, we have few opportunities to come across those cases, because modern diagnosis of colon disease could make differential diagnosis easily with the sense of broad spectrum of IBD. We presented three cases of segmental colitis and one case of so-called indeterminate colitis associated of carcinoma in the cecum and discussed the clinical significance for diagnosis and finding the step of studying the etiology of IBD. Especially, in the third case, thirteen years old man was showing the sign of early stage of Crohn disease with non-caseating granuloma in the biopsy specimen at first, the findings of the segmental ulcerative colitis with crypt abscess were seen after six months in the second examination. To observe the detail changes of the mucosal lesion in this kind of cases will present the new idea for studying the etiology of IBD.
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PMID:[Unusual form of ulcerative colitis]. 1057 37

Disease states, such as the occurrence of gastrointestinal inflammation (Crohn's disease and ulcerative colitis), can be secondary to a host of determinants that act in conjunction to bring about pathologic change. The underlying factors that mediate the development of such mucosal inflammation has recently been brought to the forefront with the advent of animal models. The examination of these animal models have given researchers a better understanding of the mechanisms involved in the pathogenesis of inflammatory bowel disease. This review discusses one such model, TNBS-colitis, and the insights that it provides into the occurrence of IBD and its future treatment.
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PMID:TNBS-colitis. 1072 77

C3H/HeJBir is a substrain of C3H/HeJ mice that was generated by selective breeding for the phenotype of spontaneous colitis. These mice show increased B cell and T cell reactivity to antigens of the enteric bacterial flora. CD4+ T cells from this strain cause colitis, when activated by enteric bacterial antigens and transferred to histocompatible severe combined immunodeficient recipients. The expression of the disease phenotype of spontaneous colitis is greatly influenced by housing conditions and probably requires an immunostimulatory enteric flora. This strain seems to carry multiple susceptibility genes for colitis as does the parental C3H/HeJ strain; the genes involved are being mapped. This strain represents a high susceptibility phenotype for colitis that is providing insight into the interactions among immune, environmental and genetic factors that can result in IBD.
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PMID:The C3H/HeJBir mouse model: a high susceptibility phenotype for colitis. 1072 78


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