[To positively exclude organic disorders. How much diagnosis needs irritable colon?].
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Adult↗
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Results for “Colitis, Microscopic”
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[Colonic spirochetosis--treatable and worth consideration. Experiences from a pediatric practice].
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Adolescent↗
Primary sclerosing cholangitis associated with massive intraabdominal lymphadenopathy.
A 40-year-old man with a history of insulin-dependent diabetes mellitus was admitted to the hospital because of jaundice and pruritus. During his evaluation the diagnosis of primary sclerosing cholangitis and "microscopic" ulcerative colitis were established. Massive intraabdominal lymphadenopathy was discovered on CT scan and histological examination eventually proved this to be follicular hyperplasia. The case herein reported documents the association of primary sclerosing cholangitis with diabetes mellitus and ulcerative colitis as well as reporting the occurrence of massive intraabdominal lymphadenopathy.
Abdomen↗
The value of electron microscope studies in diagnosing malignant change in ulcerative colitis.
Ultrastructural and histological appearances were studied in normal rectal and colonic mucosa, in the mucosa immediately adjacent to neoplasms (transitional mucosa), in neoplasms themselves, and in ulcerative colitis to try to determine whether any changes found in colitis might be recognized as premalignant. Two of the ulcerative colitis specimens showed histological evidence of premalignant change and these changes were reflected at the ultrastructural level. No electron microscopical premalignant changes were found which could not more easily be detected by simple histology, and it is concluded that attempts to detect premalignant changes in ulcerative colitis using electron microscopical techniques are likely to be unrewarding.
Colitis, Ulcerative↗
Role of NK1.1+ and AsGm-1+ cells in oral immunoregulation of experimental colitis.
NK1.1 and AsGm-1 expressing cells play a role in immunomodulation. Our purpose was to determine the role of NK1.1+ and AsGm-1+ expressing cells in the inflammatory/tolerance paradigm in experimental colitis. Oral tolerance towards colitis-extracted proteins had previously been shown to alleviate experimental colitis. Colitis was induced in C57/B6 mice by intracolonic instillation of trinitrobenzenesulfonic acid (TNBS). Oral tolerance was induced via five oral doses of proteins extracted from TNBS-colitis colonic wall. Clinical, macroscopic, and microscopic scores were used for colitis assessment. To evaluate the putative role of AsGm-1 in tolerance induction, depletion of AsGm-1 expressing cells was performed. To evaluate the mechanism of tolerance induction, liver-associated NKT lymphocytes were harvested 14 days following tolerance induction, and cultured with concanavalin A (con A) and colitis-extracted proteins. T cell subsets were measured by flow cytometry. Cytokine expression was measured by intracellular staining and enzyme-linked immunosorbent assay (ELISA). Orally tolerized mice exhibited significant alleviation of the clinical, macroscopic, and microscopic parameters of colitis, with increased CD4+ILA+/CD4+IFNgamma+ lymphocyte ratio, increased IL-4, and decreased IFNgamma and IL-12 serum levels. In contrast, orally fed mice that were AsGm-1 depleted showed evidence of severe colitis. These mice exhibited significant decreased CD4 +IL4+/CD4+IFNgamma+ ratios, and an increase in IFNgamma and IL-12, with decreased IL-4 levels. NKT cells harvested from tolerized mice secreted high levels of antiinflammatory cytokines. In contrast, in nontolerized mice, NKT cells mainly secreted proinflammatory cytokines. In a tolerized environment, both NK1.1 and AsGm-1 expressing cells are essential for disease alleviation. In contrast, in a nontolerized environment, AsGm-1 expressing cells support an antiinflammatory immune paradigm, while NKT lymphocytes support a proinflammatory shift.
Animals↗
NK 1.1+ T cell: a two-faced lymphocyte in immune modulation of the IL-4/IFN-gamma paradigm.
T lymphocytes expressing NK1.1 marker (NK1.1+) have been suggested as being important in peripheral immune modulation. Alteration of the balance between Th1 proinflammatory and Th2 anti-inflammatory cytokine-producing cells can ameliorate immune-mediated disorders. The aim of the study was to determine the role of NK1.1+ lymphocytes in the pathogenesis of tolerance and proinflammatory states and to determine their role in altering the Th1/Th2 balance in experimental colitis. Colitis was induced in C57/B6 mice by intracolonic instillation of trinitrobenzenesulfonic acid (TNBS). Mice received five oral doses of colonic proteins extracted from TNBS colitis colonic wall. Standard clinical, macroscopic, and microscopic scores were used for colitis assessment. Liver-associated lymphocytes and splenocytes were harvested 14 days following tolerance induction. Depletion of NK 1.1+ lymphocytes was performed 36 hr before lymphocyte harvesting. Lymphocytes were cultured for 12 hr with Con A and colitis extracted proteins. To evaluate the role of NK1.1+ lymphocytes in keeping a balance between immunogenic and tolerogenic subsets of cells, intracellular staining and flow cytometry assays were performed in tolerized and nontolerized mice. IL-4, IL-12, and IFN-gamma levels were measured by ELISA. Administration of mouse-derived colitis-extracted proteins ameliorated experimental colitis. Tolerized mice exhibited significant improvement in all macroscopic and microscopic parameters for colitis. Depletion of NK1.1 following tolerance induction significantly decreased the CD4(+)IL-4(+)/CD4(+)IFN-gamma(+) ratio in tolerized mice. However, depletion of NK1.1 lymphocytes in nontolerized mice increased the CD4(+)IL-4(+)/CD4(+)IFN-gamma(+) ratio, compared with nondepleted nontolerized mice. Induction of tolerance led to an increase in IL4 and a decrease in IFN-gamma levels. In the experimental colitis model NK1.1+ lymphocytes play a dual role: In the presence of peripheral tolerance they may be accountable for keeping the high CD4(+)IL-4(+)/CD4(+)IFN-gamma(+) ratio and disease alleviation. However, in nontolerized conditions they may induce a proinflammatory shift.
Administration, Oral↗
Regulatory role of the pituitary-adrenal axis in experimental colitis: effect of adrenalectomy on the clinical course and the TH1/TH2 immune profile.
BACKGROUND: The hypothalamic-pituitary-adrenal (HPA) axis plays an important role in modulating immune reactions in inflammatory bowel disease. Our aim was to assess the role of the HPA axis in the pathogenesis of immunomediated colitis in mice. METHODS: Trinitrobenzene sulfonic acid (TNBS) colitis was induced in Balb/c mice. Sham operation (sham+TNBS) or bilateral adrenalectomy (Adex+TNBS) was performed 3 days later. Control groups underwent adrenalectomy without colitis induction (Adex) or were untreated [naïve mice (Naïve)]. Mice were monitored for survival, weight loss, and macroscopic and microscopic scores of colitis. FACS analysis of CD4, CD8, natural killer T lymphocytes, and serum levels of adrenocorticotropic hormone (ACTH), corticosterone (CS), interferon-gamma (IFN-gamma), interleukin-10 (IL-10), and IL-1beta were measured. Production of prostaglandin E2 (PGE2) and binding capacity to glucocorticoid receptor (GR) in colonic mucosa were also assessed. RESULTS: By day 7 following induction of colitis there was a marked increase in ACTH and CS levels in the colitis as compared with the control group (86 +/- 6.5 pg/mL and 16 +/- 1.9 pg/mL, and 23.3 +/- 2 pg/mL and 2.8 +/- 0.8 pg/mL, respectively). There was a decrease in ACTH and CS levels by day 28 in the colitis group, but the levels were still significantly higher than the levels in controls. Adrenalectomy markedly exacerbated colitis. The macroscopic and microscopic scores increased from 2.79 +/- 0.03 and 2.0 +/- 0.1 in the sham+TNBS group to 3.3 +/- 0.3 and 3.2 +/- 0.3 in the Adex+TNBS group. Survival and weight loss correlated with these differences. A significant increase in IL-10, IFN-gamma, and PGE2 was noted in the Adex+TNBS group compared with the sham+TNBS group. Splenic CD4 lymphocytes decreased in the sham+TNBS and Adex+TNBS groups as compared with control groups (Adex and naïve). The CD8/CD4 ratio was significantly higher in the Adex+TNBS compared with the sham+TNBS group. Colitis also caused a significant decrease in the specific binding capacity of labeled dexamethasone to colonic mucosa. CONCLUSIONS: TNBS induced colitis activated the HPA axis and reduced the sensitivity of the inflamed mucosa to circulating glucocorticoids. Adrenalectomy markedly exacerbated TNBS-induced colitis. The effect was associated with changes in the peripheral CD8/CD4 ratio and with a TH1 cytokine shift. Our results suggest that adrenocortical hormones play an important role in the regulation of the immune system in experimental colitis.
Adrenalectomy↗
Spontaneous pseudomembranous colitis not associated with Clostridium difficile.
This paper describes two patients who developed macroscopically and microscopically typical pseudomembranous colitis without prior exposure to antimicrobial agents and without detectable Clostridium difficile or its toxin in the faeces.
Bacterial Proteins↗
Early expression of interferon gamma following oral antigen administration is associated with peripheral tolerance induction.
Oral tolerance is the induction of immune hyporesponsiveness to orally administered antigens. It was described in association with a decrease in interferon gamma (IFNgamma) production by activated T cells. To determine the role of IFNgamma and IL10 in immunemodulation via oral tolerization. Colitis was induced by intracolonic instillation of trinitrobenzene sulfonic acid. Treated mice received five oral doses of colitis-extracted proteins (CEPs) every other day, starting immediately after colitis induction. Control mice received similar doses of bovine serum albumin. Colitis was assessed in both groups by standard clinical, micro- and macroscopic scores. IFNgamma and IL10 expression in splenic lymphocytes from both groups was tested by RT-PCR immediately after oral feeding, 1, 4, 8, 12, and 24 h thereafter and then every 24 h for 2 weeks. Feeding of CEPs markedly ameliorated experimental colitis. These mice gained weight and showed markedly improved macro- and microscopic parameters of colitis. Tolerized mice exhibited IFNgamma expression in splenic lymphocytes starting immediately following oral CEP immunization and up to 14 d thereafter. IL10 was expressed starting 1 h after CEP feeding and during the first 48 h thereafter. In contrast, non-tolerized control mice manifested IFNgamma expression starting on day 6 and had no IL10 expression. Early induction of IFNgamma expression by oral antigen may be associated with systemic tolerance in the experimental colitis setting. In contrast, late expression of IFNgamma is associated with a pro-inflammatory response in non-tolerized controls.
Administration, Oral↗
The role of intrahepatic CD8+ T cell trapping and NK1.1+ cells in liver-mediated immune regulation.
UNLABELLED: The liver was previously suggested as a site of lymphocyte clearance. Liver-associated lymphocytes that express NK1.1 marker (NKT LAL) play a role in immune modulation. AIM: To determine the role of the liver and of NKT LAL in determining the CD4+/CD8+ balance during tolerance induction. METHODS: Colitis was induced in C57 mice by intracolonic instillation of trinitrobenzenesulfonic acid (TNBS). Immune tolerance was induced via five oral feedings of colitis-extracted proteins (CEP) from TNBS-colitis colonic wall, starting on the day of colitis induction (group A). Control mice were fed with BSA (group B). To determine the role of NKT cells in immune modulation, NK1.1 depletion was performed in nonfed (group C) and fed (group D) mice. To further evaluate the role of NKT cells in this model, mice in group E were tolerized following NKT depletion. To determine the effect of NKT depletion in a tolerized environment, tolerized mice in group F were NKT depleted following tolerance induction. Peripheral and intrahepatic NK1.1+ and CD4+/CD8+ T cells were determined in all groups. Colitis was assessed by standard clinical and histologic scores. Serum cytokines levels were measured by ELISA. RESULTS: Oral tolerance induction led to a marked alleviation of colitis as manifested by a significant improvement of the clinical, macroscopic, and microscopic scores of colitis (group A vs. group B). NK1.1+ depletion without tolerance induction had a favorable effect on colitis (C). Depletion of NKT LAL prevented the ability to induce tolerance (group D). However, induction of tolerance following NK1.1+ depletion, and NK1.1+ depletion following tolerance induction led to a marked improvement of colitis (groups E and F). Tolerance induction led to a significant increase in NKT LAL numbers. The peripheral CD4+/CD8+ ratio increased up to 3-fold in tolerized vs. non-tolerized mice. A similar increase was observed in NKT-depleted healthy mice in groups C, E, and F (P < 0.005). In contrast, NK1.1+ depletion in the presence of antigen in the bowel led to a reverse effect with a significant decrease in the peripheral CD4+/CD8+ ratio. An opposite effect was observed in the intrahepatic CD4+/CD8+. The peripheral/intrahepatic CD4+/CD8+ ratio increased significantly in tolerized and in healthy mice (A, D, E, F, P < 0.005). In contrast, NK1.1+ depleted fed mice in group C manifested a marked decrease in the peripheral/intrahepatic CD4+/CD8+ ratio. Induction of tolerance led to a marked increase in the IL-10/interferon gamma (IFNgamma) and IL-4/IFNgamma ratios. CONCLUSIONS: In the experimental colitis model, the liver is an important site for CD8+ accumulation during tolerance induction in a process that is independent of NK1.1+ cells. NK1.1+ cells play a dual role in the pro/anti-inflammatory balance. In the presence of antigen, these lymphocytes may be accountable for keeping an anti-inflammatory lymphocyte balance. However, in the absence of antigen, they may induce a pro-inflammatory shift.
Animals↗
Diversion colitis: a trigger for ulcerative colitis in the in-stream colon?
The aetiology of ulcerative colitis is unknown. Two patients without pre-existing inflammatory bowel disease in whom end colostomy for faecal incontinence was complicated by diversion colitis in the defunctioned rectosigmoid colon, are described. In both instances, colitis with the clinical, colonoscopic, and microscopic features of ulcerative colitis developed about a year later in the previously normal in-stream colon proximal to the colostomy. These cases suggest that diversion colitis may be a risk factor for ulcerative colitis in predisposed individuals and that ulcerative colitis can be triggered by anatomically discontinuous inflammation elsewhere in the large intestine.
Adolescent↗
Fulminant colitis in inflammatory bowel disease: detailed pathologic and clinical analysis.
PURPOSE: The morphologic features of fulminant colitis may be nonspecific, making differentiation between ulcerative colitis and Crohn's disease difficult, even after colectomy. The aims of this study were 1) to identify histologic features that accurately differentiated ulcerative colitis, Crohn's disease, and indeterminate colitis in fulminant colectomy specimens; 2) to determine how frequently subsequent clinical course altered the pathologic diagnosis; and 3) to evaluate the natural history of histologically diagnosed indeterminate colitis. METHODS: Ninety-five fulminant colectomy specimens were evaluated, of which 85 had an original diagnosis of fulminant inflammatory bowel disease. Complete pathologic material and comprehensive clinical follow-up information was available on 67 cases of inflammatory bowel disease. These were re-evaluated in a blinded fashion, and histopathologic features were compared with the original diagnosis and reviewed in the light of subsequent clinical behavior to reach a final diagnosis. RESULTS: Evaluation of macroscopic features was not helpful in differentiating ulcerative colitis from Crohn's disease. Microscopic examination correctly diagnosed ulcerative colitis or Crohn's disease in only 58 of 67 (87 percent) cases. A further three cases (4 percent) were definitively classified after correlation with clinical data, leaving a residual six cases that were diagnosed as indeterminate colitis. Granulomas and lymphoid aggregates were the two most specific indicators of Crohn's disease. CONCLUSIONS: Histopathologic evaluation alone has limitations in the accurate classification of fulminant inflammatory bowel disease. Histologically diagnosed indeterminate colitis is a heterogeneous group that may include some patients who subsequently prove to have ulcerative colitis or Crohn's disease.
Adolescent↗
Ulcerative colitis in protracted remission. A quantitative scanning electron microscopic study.
Colonoscopic biopsies from 32 patients were studied at the ultrastructural level using a scanning electron microscope (SEM). Sixteen of the 32 patients had a previous diagnosis of total ulcerative colitis (UCR greater than 10 years) in protracted remission. The colonic mucosa was normal at endoscopic and histologic examinations (UCRN). The remaining 16 patients had normal colonic mucosa, but had an adenoma or an adenocarcinoma elsewhere in the colon. Several ultrastructural parameters were investigated, such as the number of crypts per area, the distance between the crypts, the outline of mucosal units, the number of mucous cells, the outline of absorptive cells, and the number of villi per area. Quantitative determinations of SEM structures (including measurements with an interactive digital image analyzer system; MOP 30, Zeiss Contron) were made. The results showed no significant differences between the various parameters (except for the number of crypts per area) between patients with UCRN and controls. The possibility of a total (or quasi-total) restitutio ad integrum of the colonic mucosa in certain patients with UCR is discussed. An international policy regarding the colonoscopic surveillance of patients with UCRN should be elaborated. It is suggested that the time interval between control colonoscopic biopsies in patients with UCRN should be increased substantially.
Adenocarcinoma↗
Colitis: problems in pathologic and clinical diagnosis: indeterminate, microscopic, and diverticulitis. Yale University Workshop Report. October, 2003. Norwalk, Connecticut, USA.
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Colitis↗
Fumigaclavine C, an fungal metabolite, improves experimental colitis in mice via downregulating Th1 cytokine production and matrix metalloproteinase activity.
In the present paper, the effect of Fumigaclavine C, a fungal metabolite, on experimental colitis was examined. Fumigaclavine C, when administered intraperitoneally once a day, significantly reduced the weight loss and mortality rate of mice with experimental colitis induced by intrarectally injection of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS). This compound also markedly alleviated the macroscopic and microscopic appearances of colitis. Furthermore, Fumigaclavine C, given both in vivo and in vitro, showed a marked inhibition on the expression of several inflammatory cytokines, including IL-1beta, IL-2, IL-12alpha, IFN-gamma, TNF-alpha as well as MMP-9 in sacral lymph node cells, colonic patch lymphocytes and colitis tissues from the TNBS colitis mice. Meanwhile, the compound caused a dose-dependent reduction in IL-2 and IFN-gamma from the lymphocytes at the protein level and MMP-9 activity. These results suggest that Fumigaclavine C may alleviate experimental colitis mainly via down-regulating the production of Th1 cytokines and the activity of matrix metalloproteinase.
Acremonium↗
Unusual colitides.
Colitis is an important cause of abdominal pain and diarrhoea and is the main cause of blood and mucus in the stool. The inflammation can be due to infectious or to non-infectious causes, most commonly ulcerative colitis and Crohn's disease. However, a wide variety of rarer causes of colitis also present in childhood. These include colitis or enterocolitis secondary to Hirschsprung's disease and metabolic disorders (which include Hermansky-Pudlak syndrome, glycogen storage disease type 1b and pellagra). Primary inflammation of the colon is seen in microscopic and collagenous colitis, ulcerating enterocolitis of infancy, allergic colitis and autoimmune enteropathy. The histological pattern of each of these diseases has a characteristic picture and separates them from each other from ulcerative colitis and Crohn's disease. The pathophysiology of these rare forms of colitis in childhood is not clear; but in the future they may give us an insight into the pathogenesis of large bowel inflammation, particularly when the colitis occurs secondary to an established disease.
Child↗
Preferential migration of CD62L cells into the appendix in mice with experimental chronic colitis.
BACKGROUND: Clinical and experimental studies suggest that appendectomy can protect against development of ulcerative colitis and Crohn's disease. However, how T cells in the appendix affect the development of colitis has not been clarified. AIM: To investigate the in vivo migration and activation of colitis-inducing CD62L+ cells during development of chronic colitis. METHODS: CD62L+CD4+ cells were fluorescently labeled and transferred to severe combined immunodeficient (SCID) mice to induce colitis. In vivo migration of T cells into the mucosa of the appendix and colon was quantified by in vivo microscopy after 7 weeks. In a second experiment, unlabeled CD62L+CD4+ cells were transferred, reisolated after 7 weeks, and adhesion molecule (integrin alpha4beta7) and costimulatory molecule (CD154) expression was analyzed. RESULTS: Six to eight weeks after CD62L+CD4+ cell transfer, SCID mice developed chronic colitis. In vivo microscopic analysis demonstrated a preferential migration of fluorescence-labeled CD62L+CD4+ cells into the mucosa of the appendix versus the colon. Re-isolation of lamina propria cells from mice with colitis confirmed that CD62L+CD4+ cell migration was significantly enhanced in the appendix, compared to the colon (3.5-fold). Furthermore, a higher proportion of CD62L+CD4+ cells re-isolated from the appendix expressed integrin alpha4beta7 and CD154 than from the colon. CONCLUSION: This study demonstrates the preferential migration of CD62L+CD4+ cells into the appendix as compared to the colon. This migration pattern correlated with upregulation of integrin alpha4beta7 and CD154 (CD40 ligand) on T cells. Our results suggest an important role of the appendix in the pathogenesis of colitis.
Adoptive Transfer↗