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PubMed1976

Immunosuppression in the treatment of inflammatory bowel disease. II. The effects of azathioprine on lymphoid cell populations in a double blind trial in ulcerative colitis.

Blood lymphocytes and rectal plasma cells have been studied in patients with ulcerative colitis taking part in a double-blind trial of treatment with azathioprine. Treatment for 1 year resulted in a modest fall in blood lymphocyte count, with little change in neutrophils or platelets. There was no major change in the proportions of circulating T and B lymphocytes, suggesting that the number of such cells per millilitre of blood fell in proportion to the change in lymphocyte count. The number of plasma cells in the rectal lamina propria was reduced to a mean less than half that of the control patient group. Blood K-cell cytotoxic activity fell at least 25-fold after 1 year's treatment. PHA-induced cytotoxicity was also reduced, but less consistently. Reduced K-cell activity is interpreted as reflecting depletion of effector cells from the circulation. The fall in lymphocyte count, K-cell activity and gut plasma cells was slow, indicating continuous inhibition of lymphopoiesis or differentiation throughout the trial period. Thus, azathioprine has some immunosuppressive effects which develop only after prolonged treatment. The clinical results of the trial did not show a major beneficial effect of azathioprine in the treatment of ulcerative colitis, nor were there clear correlations between the results of lymphocyte assays and clinical response in individual patients.

Antibody-Producing Cells↗
PubMed2001

HLA class-I-restricted and colon-specific cytotoxic T cells from lamina propria lymphocytes of patients with ulcerative colitis.

We established cytotoxic T-lymphocyte (CTL) lines against colonic epithelial cell line from LPLs of patients with ulcerative colitis by continuous stimulation with human lymphocyte antigen A (HLA-A) matched colonic epithelial cell lines and clones from LPLs using polyclonal stimulation with phytohemagglutinin. The established CTL lines and clones showed cytotoxicity against HLA-A-matched colonic epithelial cell line but not against HLA-mismatched colonic epithelial cell lines, and HLA-A-matched lung and esophagus cell lines. The CTL response was HLA class I-restricted and mediated by CD8-positive T-lymphocytes. Moreover, the CTL line showed cytotoxicity against autologous B-LCLs pulsed with peptides extracted from HLA-A-matched colonic epithelial cell line but not against other organ-derived peptides pulsed and unpulsed autologous B-LCLs. CTL lines and clones established from LPLs of patients with ulcerative colitis showed colon-specific and HLA class I-restricted killing of human colonic epithelial cell line, suggesting that these CTLs may play a role in colonic epithelial cell damage in some patients with ulcerative colitis.

Adult↗
PubMed1998

Lymphoid hyperplasia, autoimmunity, and compromised intestinal intraepithelial lymphocyte development in colitis-free gnotobiotic IL-2-deficient mice.

IL-2-deficient (IL-2(-/-)) mice develop disorders of the hemopoietic and immune systems characterized by anemia, lymphocytic hyperplasia, and colitis. The mechanisms responsible for these abnormalities remain unclear. To investigate the underlying basis of autoimmunity, the particular role of commensal gut flora in the initiation of colitis, and the role of IL-2 in the development of intestinal intraepithelial lymphocytes (iIEL), we evaluated IL-2(-/-) mice reared and maintained under gnotobiotic (germfree) conditions. By 8 wk of age, 80% (20 of 25) of germfree IL-2(-/-) mice show signs of disease, including anemia, disturbances in bone marrow hemopoietic cells, lymphocytic hyperplasia, and generalized autoimmunity, similar to those seen in specific pathogen-free (SPF) IL-2(-/-) mice. In striking contrast to SPF IL-2(-/-) mice, germfree IL-2(-/-) mice do not develop colitis. However, the numbers of gammadelta+ and TCR alphabeta+ CD8 alphaalpha+ iIELs are reduced, and in lethally irradiated SPF IL-2(+/+) mice, reconstituted with IL-2(-/-) bone marrow TCR gammadelta+ iIELs fail to develop, consistent with an important role of IL-2/IL-2R signaling in the development of gammadelta iIELs. Consequently, our findings demonstrate that the colitis seen in SPF IL-2(-/-) mice depends upon the presence of intestinal bacterial flora and that environmental Ags are not responsible for the anemia and extraintestinal lymphoid hyperplasia that occur in IL-2(-/-) mice. Thus, germfree IL-2(-/-) mice represent a unique system in which the role of IL-2 deficiency in hemopoietic and immune system disorders can be investigated in dissociation from complications that may arise due to colitis.

Age Factors↗
PubMed1981

Dinitrochlorobenzene-induced colitis in the guinea-pig: studies of colonic lamina propria lymphocytes.

Dinitrochlorobenzene-induced colitis in guinea-pigs may be immunologically mediated: animals must be presensitised to dinitrochlorobenzene to develop colitis, sensitivity can be passively transferred by lymphocytes and the injury can be mitigated by immunosuppression. In this study, we examined lamina propria lymphocytes isolated from colons of animals with dinitrochlorobenzene-induced colitis, and appropriate controls. Lamina propria lymphocytes from colitis animals have a greater percentage of rabbit erythrocyte-rosetting cells (T cells) (20.1 +/- 3.0 vs 2.3 +/- 0.8, p less than .01) and a greater capacity to mediate mitogen-induced cellular cytotoxicity with phytohaemagglutinin than lamina propria lymphocytes from normal colon (% specific cytoxicity = 29.4 +/- 8.7 vs 5.0 +/- 4.5, P less than .005). There was no difference in the percentage of rosetting cells or cytotoxicity index of spleen or mesenteric lymph node lymphocytes between the colitis animals and controls. These data suggest that there are changes in the distribution and functional characteristics of lamina propria lymphocytes which correlate with mucosal cell injury in the dinitrochlorobenzene-colitis model.

Animals↗
PubMed1991

Two-color immunofluorescence and flow cytometric analysis of lamina propria lymphocyte subsets in ulcerative colitis and Crohn's disease.

By using two-color immunofluorescence with fluorescein isothiocyanate (FITC) and phycoerythrin (PE)-labelled monoclonal antibodies and multiparameter flow cytometry, we investigated lamina propria lymphocyte subsets of patients with ulcerative colitis (UC) and Crohn's disease (CD). Leu-3/Leu-2 (CD4/CD8) ratio of lamina propria lymphocytes (LPL) of CD (mean +/- SD: 1.9 +/- 0.8, P less than 0.01) was significantly decreased compared with controls (3.3 +/- 1.1), because of an increased number of CD8+ lymphocytes. The majority of lamina propria CD4+ cells were CD4+, Leu-8- and CD4+, CD45R- both in controls and IBD tissue. Many lamina propria T lymphocytes were activated, expressing HLA-DR antigen not only in IBD but also in controls. NK cells defined by CD16 and CD 56 (3.0 +/- 1.4%, P less than 0.01) were significantly decreased in patients with UC compared with controls (6.5 +/- 3.0%). A low proportion of B cells in the intestinal mucosa expressed Leu-8 antigen and CD23 antigen. The proportion of activated B cells of LPL was high in IBD mucosa as well as normal mucosa. These findings suggest that local activation of B cells leads to the loss of the expression of Leu-8 antigen and CD23.

Adolescent↗
PubMedDate not supplied

Prevalence of microscopic colitis in patients with symptoms suggesting irritable bowel syndrome.

GOALS/BACKGROUND: Irritable bowel syndrome is a common disorder affecting 20% of the general population. It shows certain characteristics with organic bowel diseases. Definition of lymphocytic and collagenous colitis has created a new approach towards chronic idiopathic diarrheas. We searched for the frequency of lymphocytic and collagenous colitis in patients with irritable bowel syndrome. STUDY: The study group consisted of 30 irritable bowel patients and 20 controls. Multiple biopsies from cecum; ascendant, transverse and descendent colon; sigmoid and rectum were taken sequentially in all patients. RESULTS: We diagnosed 7 out of 30 irritable bowel patients as having lymphocytic colitis (23.3%) but none as having collagenous colitis. In the control group 1 out of 20 patients had lymphocytic colitis (5%) and none had collagenous colitis. Irritable bowel patients had higher rate of lymphocytic colitis association (p < 0.05). CONCLUSIONS: Functional disorders of the bowel should be searched for possible lymphocytic colitis, especially in cases refractory to classical therapies.

Adult↗
PubMed1998

High Fas ligand expression on lymphocytes in lesions of ulcerative colitis.

BACKGROUND: The pathogenesis of ulcerative colitis is unclear, but cytotoxic T lymphocytes infiltrating the mucosa have been implicated in mucosal damage. The Fas ligand (FasL), expressed on cytotoxic T lymphocytes, induces apoptosis in cells expressing Fas. AIM: To analyse FasL expression in affected colonic mucosa to ascertain Fas-FasL interaction in ulcerative colitis. METHODS: FasL mRNA was quantified in colonic mucosal specimens from healthy subjects and patients with ulcerative colitis or Crohn's disease, using the competitive reverse transcription polymerase chain reaction. FasL mRNA localisation was determined by in situ hybridisation. Expression of Fas in colonic mucosa was analysed immunohistochemically. Phenotypes of lamina propria lymphocytes that expressed FasL were analysed by flow cytometry. RESULTS: FasL mRNA was strongly expressed in active ulcerative colitis lesions, but not in those associated with active Crohn's disease or active proctitis-type ulcerative colitis. In situ hybridisation showed that FasL mRNA expression occurred in mononuclear cells infiltrating lesions. Fas was expressed in epithelial cells in ulcerative colitis and Crohn's disease, and in normal subjects. Cytometry showed that FasL was expressed in CD3 lymphocytes infiltrating the lamina propria in active lesions. CONCLUSIONS: FasL is expressed in CD3 lymphocytes infiltrating into ulcerative colitis but not Crohn's disease lesions, suggesting that Fas-FasL induced apoptosis participates in the mucosal damage of ulcerative colitis.

Acute Disease↗
PubMed1980

Cytotoxic effect in vitro of B lymphocytes and killer (K) cells in ulcerative colitis.

A mixture of B lymphocytes and K cells was isolated from serum of 18 patients suffering from ulcerative colitis (U.C.) and of 10 healthy individuals constituting the control group. The cytotoxic effect of these cells in vitro on the large bowel epithelial cells was examined. It was found that the mixture of B lymphocytes and K cells obtained from the patients suffering from ulcerative colitis destroyed the epithelial cells of large bowel, and that the cytotoxic effect depended primarily upon a degree of the severity of the disease. The results obtained confirmed our suggestion that B lymphocytes and K cells cooperate directly in the cytotoxic reaction.

Antibody-Dependent Cell Cytotoxicity↗
PubMed2005

Increased lymphocyte trafficking to colonic microvessels is dependent on MAdCAM-1 and C-C chemokine mLARC/CCL20 in DSS-induced mice colitis.

Although enhanced lymphocyte trafficking is associated with colitis formation, little information about its regulation is available. The aim of this study was to examine how the murine liver and activation-regulated chemokine (mLARC/CCL20) contributes to lymphocyte recruitment in concert with vascular adhesion molecules in murine chronic experimental colitis. T and B lymphocytes isolated from the spleen were fluorescence-labelled and administered to recipient mice. Lymphocyte adhesion to microvessels of the colonic mucosa and submucosa was observed with an intravital microscope. To induce colitis, the mice received two cycles of treatment with 2% dextran sodium sulphate (DSS). In some of the experiments antibodies against the adhesion molecules or anti-mLARC/CCL20 were administered, or CC chemokine receptor 6 (CCR6) of the lymphocytes was desensitized with excess amounts of mLARC/CCL20. Significant increases in T and B cell adhesion to the microvessels of the DSS-treated mucosa and submucosa were observed. In chronic colitis, the accumulation of lymphocytes was significantly inhibited by anti-mucosal addressin cell adhesion molecule (MAdCAM)-1 mAb, but not by anti-vascular cell adhesion molecule-1. In DSS-treated colonic tissue, the expression of mLARC/CCL20 was significantly increased, the blocking of mLARC/CCL20 by monoclonal antibody or the desensitization of CCR6 with mLARC/CCL20 significantly attenuated the DSS-induced T and B cell accumulation. However, the combination of blocking CCR6 with MAdCAM-1 did not further inhibit these accumulations. These results suggest that in chronic DSS-induced colitis, both MAdCAM-1 and mLARC/CCL20 may play important roles in T and B lymphocyte adhesion in the inflamed colon under flow conditions.

Animals↗
PubMed1992

Phenotypic characterization of isolated intraepithelial lymphocytes in patients with ulcerative colitis and normal controls.

A method was developed to isolate colonic intraepithelial lymphocytes in patients with ulcerative colitis (N = 8) and normal controls (N = 13) in order to characterize their phenotype using a panel of monoclonal antibodies and flow cytometry. In both groups, the majority of the cells are of the CD3+CD8+ phenotype associated with cytotoxic/suppressor function. The CD4/CD8 ratios were similar. Virtually no B cells or macrophages were found. An increase in cells coexpressing the CD3 and HLA-DR molecules and a decrease in natural killer cells (CD3, CD16+CD56+) were found in ulcerative colitis, but this was not significant. There were no differences in the proportions of CD8+ and CD4+ cells expressing the Leu8 antigen between ulcerative colitis and controls. Thus a population of colonic intraepithelial lymphocytes has been isolated and, although they may be functionally different in ulcerative colitis compared with controls, this cannot be explained in terms of phenotypic characteristics.

Adult↗
PubMedDate not supplied

Chronic colitis in Macaca fascicularis: similarities with chronic colitis in humans.

In recent years, a substantial number of macaques have died at the Southwest Foundation for Biomedical Research, USA, following protracted intractable diarrhea. The diarrhea could last for up to two years and occurred in infant, juvenile or young adult animals. The histopathological diagnosis at autopsy was chronic colitis. The histopathological subtype of chronic colitis is here assessed in a relatively large number of colonic specimens obtained at autopsy (n = 90). The colonic mucosa was well preserved for histological examination in 83 of the 90 macaques. At review, various histological phenotypes of chronic colitis were found. Chronic lymphocytic-plasmacytic colitis occurred in 78.3% (65 out of 83), chronic ulcerative colitis in 20.5% (17 out of 83) and Crohn's colitis in 1.2% (1 out of 83). In macaques, some histological phenotypes of chronic colitis (ulcerative and Crohn's colitis) closely mimic chronic colitis in humans. The awareness that chronic colitis in macaques is not one disease but a series of chronic inflammatory changes, with common clinical symptoms and similar gross appearances, may lead to the correct histological diagnosis of the subtype of the disease.

Animals↗
PubMed1994

Crohn's disease, ulcerative colitis, and normal intestinal lymphocytes express integrins in dissimilar patterns.

BACKGROUND/AIMS: The integrin family of adhesion molecules on intestinal lamina propria mononuclear cells (LPMNC) was studied using fluorescence-activated cell cytometry. These molecules are implicated in extravascular cell migration and are important regulators of disease. METHODS: Using fluorescence-activated cell cytometry, B- and T-cell subsets in the intestines of 10 normal patients, 11 patients with Crohn's disease, and 8 patients with ulcerative colitis were stained with monoclonal antibodies to a panel of integrins. RESULTS: Expression of alpha integrins on CD3+ T cells and CD19+ B cells was different in normal and inflammatory bowel disease LPMNC. Ulcerative colitis T cells expressed less beta 1 and alpha 4 and significantly more alpha 2 and alpha 6. There was a difference in alpha 4 and beta 1 expression between LPMNC B cells from Crohn's disease and normal intestines. Sixteen percent of CD19+ LPMNC B cells from Crohn's and 19% of ulcerative colitis LPMNC expressed alpha 2. Crohn's and ulcerative colitis CD19+ LPMNC B cells expressed more alpha 5 integrin than normal specimens. CD3+ T cells and CD19+ B cells expressed alpha 6 only in ulcerative colitis. Ulcerative colitis and Crohn's disease CD19+ LPMNC expressed less alpha 4, consistent with their reciprocal increases of alpha 5 and alpha 2. A difference in beta 7 (Peyer's patch specific) antigen was observed between inflammatory bowel disease and normal LPMNC for both CD3+ and CD19+ LPMNC. CONCLUSIONS: These findings identify the differences of lymphocyte homing capability in inflammatory bowel disease and normal intestine.

Antigens, CD↗
PubMed2004

Microscopic colitis.

Microscopic colitis (MC) is viewed as an umbrella term applicable to both lymphocytic and collagenous colitis. The first case was published in 1976, a new entity with chronic watery diarrhea with lymphocytic colitis, with or without a subepithelial collagen deposition. Patients are usually middle-aged women, and the pathogenesis is unknown. The response to steroids and the female predominance underlines an autoimmune disease. Up to 40% NSAID's and Lanzoprazole-induced MC are well-known. Biopsies during sigmoidoscopy in unexplained diarrhea must be standard. Treatment is empirical. The most important step is to ban all NSAID's and other MC inducing agents. Immunosuppressive treatment must be considered. However the disease has a benign course and sometimes is selflimiting.

Colitis↗
PubMed2005

Adoptive transfer of NK 1.1+ lymphocytes in immune-mediated colitis: a pro-inflammatory or a tolerizing subgroup of cells?

UNLABELLED: T lymphocytes expressing NK1.1 marker (NKT) have been suggested to play crucial roles in immune modulation. AIM: To determine the role of NK1.1+ cells in induction and maintenance of pro-inflammatory and/or tolerizing responses. METHODS: Colitis was induced in C57/B6 donor mice by intracolonic instillation of trinitrobenzenesulfonic acid (TNBS). Donor mice received five oral doses of colonic proteins extracted from TNBS-colitis colonic wall. Depletion of NK1.1+ lymphocytes was performed before lymphocyte harvesting. Splenocytes were harvested and separated into T-cell subpopulations, and transplanted into recipient mice before intracolonic instillation of TNBS. Standard clinical, macroscopic, and microscopic scores, and intracellular staining, flow cytometry, and cytotoxicity assays were performed. RESULTS: The adoptive transfer of CD4+ and NK1.1+ cells harvested from tolerized mice markedly ameliorated the colitis in recipient mice. In contrast, the adoptive transfer of CD8+ and double negative lymphocytes failed to transfer the tolerance. Recipients of splenocytes from tolerized mice exhibited an increase in CD4+ IL4+/CD4+ IFNgamma+ ratio. In contrast, recipients of splenocytes from NK1.1-depleted-tolerized mice exhibited severe colitis with a significant decrease of the CD4+ IL4+/CD4+ IFNgamma+ ratio. However adoptive transfer of splenocytes from non-tolerized NKT-depleted mice led to an alleviation of colitis with a relative increase of the CD4+ IL4+/CD4+ IFNgamma+ ratio. CONCLUSIONS: NK1.1+ lymphocytes play a critical role in immune regulation. They may be accountable for an alteration of the inflammatory response and the CD4+ IL4+/CD4+ IFNgamma ratio immune-mediated colitis and in peripheral tolerance induction.

Adoptive Transfer↗
PubMed2004

Sudden onset of colitis after ablation of secretin-expressing lymphocytes in transgenic mice.

Though secretin mRNA was demonstrated in mouse lymphoid organs, its role in the immune system is unknown. Here, secretin gene-expressing cells were ablated by ganciclovir infusion in mice transgenic for the rat secretin promoter (Sec) directing the expression of herpesvirus thymidine kinase (Sec-HSVTK). Thymus, spleen, blood, and colon were investigated by histology. Lymphoid cells were extracted and quantified, and CD19+ B-cells and CD3+, CD103+, CD4+, and CD8+ T-cells were analyzed by flow cytometry. Protein extracts from spleen and thymus were assayed for secretin by Western blotting, and isolated lymphocytes were investigated for HSVTK, secretin, and secretin receptor (Sec-R) mRNA by reverse transcription-polymerase chain reaction (RT-PCR). Ablation of secretin-expressing cells produced severe colitis with morphological features similar to those observed in graft-versus-host (GVH) disease. Profound lymphoid depletion was observed in spleen, thymus, and peripheral blood. The relative percentage of B- and T-cell subsets were unaffected. Analysis of colonic lymphocytes revealed a marked depletion of CD4+ T lymphocytes. Colitis and lymphoid depletion were not reversed by secretin cotreatment. Immunoblot analysis of protein extracts from spleen and thymus identified secretin-like immmunoreactant. RT-PCR of lymphocyte mRNA from spleen and thymus identified secretin and secretin receptor transcripts. We conclude that GVH-like colitis in ganciclovir-treated Sec-HSVTK mice arises from depletion of secretin gene-expressing lymphoid cells and not from the failure of secretin production.

Animals↗
PubMed2002

Synergistic inhibitory effect of cyclosporin A and vitamin D derivatives on T-lymphocyte proliferation in active ulcerative colitis.

OBJECTIVE: 1,25-Dihydroxyvitamin D3 [1,25(OH)2D3], the hormonal active form of vitamin D3, could represent a potentially therapeutic agent in autoimmune diseases. Cyclosporin A (CsA) shows immunoregulatory properties, which, in many respects, seem to be similar to those of 1,25(OH)2D3. Our aim was to investigate the possible synergistic effect exerted by CsA in combination with 1,25(OH)2D3 or its nonhypercalcemic analogues, EB 1089 and KH 1060, on the proliferative response of T lymphocytes obtained from active ulcerative colitis patients. METHODS: The T lymphocyte-enriched population was treated with phytohemagglutinin and CsA (doses from 1 ng to 1000 ng/ml) alone or in association with 1,25(OH)2D3 or EB 1089 or KH 1060 (0.1, 1, 10 nM final concentration). Cell proliferation was determined by [3H]thymidine incorporation and analyzed on day 5 of culture. RESULTS: After incubation with CsA, T lymphocyte proliferation was significantly inhibited in comparison with the vehicle-treated cultures. However, T lymphocytes from ulcerative colitis patients were significantly more sensitive to CsA than those from healthy controls. The inhibition in T lymphocyte proliferation, after treatment of the cultures with CsA associated with either 1,25(OH)2D3 or EB 1089 or KH 1060, was synergistic at well-defined concentrations. CONCLUSIONS: Taking into account the lowest CsA dose (1 ng/ml), the highest synergistic inhibition in the proliferation of T lymphocytes prepared from ulcerative colitis patients was found combining CsA and 10 nM of 1,25(OH)2D3 or 10 nM of EB 1089 or KH 1060 at the three concentrations. The results obtained, associating the lowest CsA dose and the lowest KH 1060 concentration, may suggest an alternative therapeutic approach in these patients, reducing the dose, and consequently the toxicity, of CsA.

Adult↗
PubMedDate not supplied

Inflammatory bowel disease with cytoplasmic-staining antineutrophil cytoplasmic antibody and extensive colitis.

A cohort of 18 patients with inflammatory bowel disease who were characterized by the presence of cytoplasmic-staining antineutrophil cytoplasmic antibody (cANCA) and extensive colitis is reported. Almost half were Indo-Canadians, and atypical perinuclear-staining antineutrophil cytoplasmic antibody was also detected in five (28%), similar to the detection rate for Crohn's disease and other less commonly detected forms of colitis, such as lymphocytic or collagenous colitis. Careful pathological review of all endoscopic biopsies and surgically resected colonic tissues did not reveal evidence of vasculitis or so-called 'palisading' granulomas, which is a typical pathological change of Wegener's granulomatosis, an entity that has been traditionally characterized by the detection of cANCA. This report describes 18 patients with extensive colitis and the seromarker cANCA but without clinical features or histological evidence of vasculitis.

Adolescent↗