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PubMedDate not supplied

Nodular duodenitis involving CD8+ cell infiltration in patients with ulcerative colitis.

BACKGROUND/AIMS: Limited efforts have been made to determine changes in the upper gastrointestinal tract in ulcerative colitis. The aim of this study was to analyze gastroduodenal lesions in patients with ulcerative colitis. METHODOLOGY: The endoscopical appearance of lesions in the duodenum and stomach was first examined. Biopsy specimens taken from 25 patients with ulcerative colitis, as well as 21 with Crohn's disease and 16 with nonspecific gastroduodenitis who had no Helicobacter pylori infection, were then evaluated by histology and immunohistochemistry for CD8, CD68 and HLA-DR. In ulcerative colitis patients, the HLA-phenotype was also analyzed by the standard NIH complement-dependent microlymphocyte toxicity assay. RESULTS: Endoscopically evident alteration of nodularity in the descending part of duodenum was prominent in ulcerative colitis and Crohn's disease, but not gastroduodenitis. Histological inflammatory change of the duodenal bulb in ulcerative colitis and Crohn's disease was mild as compared to gastroduodenitis cases. Endoscopic and histological change (redness and deformity of villi) in the duodenum were more prominent in ulcerative colitis patients with pancolitis than those with left-sided/proctitis. CD8+ cells infiltrating both the duodenum and stomach were increased in ulcerative colitis and Crohn's disease as compared to gastroduodenitis whereas focal perifoveolar accumulation of CD68+ cells and enhanced epithelial expression of HLA-DR were characteristic of Crohn's disease. Histopathological alteration in the duodenum was particularly prevalent in ulcerative colitis patients with HLA-DR4 and Cw1. CONCLUSIONS: Nodular, histologically mild duodenitis involving CD8+ cell infiltration, the severity of which positively correlates with the extent of colitis, is characteristic of ulcerative colitis.

Adolescent↗
PubMed1991

Loss of interleukin-2-producing intestinal CD4+ T cells in inflammatory bowel disease.

Interleukin-2 activity of intestinal lamina propria mononuclear cells is decreased in Crohn's disease and ulcerative colitis patients compared with control patients with noninflammatory bowel disease. Factors that might be responsible for this phenomenon were investigated. Most interleukin-2 activity was produced by helper (CD4+) T cells. These were present in comparable numbers in both inflammatory bowel disease and control cultures, but the frequency of interleukin-2-producing cells was significantly (3-4 times) lower among Crohn's disease and ulcerative colitis than control cells. In agreement with this finding, levels of interleukin-2 messenger RNA were substantially decreased in both forms of inflammatory bowel disease compared with controls. Mucosal CD8+ T cells and plastic-adherent cells were unable to suppress interleukin-2 activity by autologous or allogeneic CD4+ T cells. The rate of interleukin-2 absorption was similar for inflammatory bowel disease and control cells. Induction of interleukin-2 by different stimuli (phorbol ester, phytohemagglutinin, or anti-CD3 monoclonal antibody) before or after incubation under basal conditions ("resting") failed to normalize the capacity to generate interleukin-2 by Crohn's disease and ulcerative colitis cells. Prostanoids (prostaglandin E2 and 6-keto-prostaglandin F1 alpha) were produced in large amounts in cultures of inflammatory bowel disease cells, but inhibition by indomethacin failed to restore interleukin-2 activity to control levels. Finally, supernatants from Crohn's disease and ulcerative colitis cell cultures failed to suppress interleukin-2 production by control CD4+ T cells. Our results show that the low interleukin-2 activity detected in inflammatory bowel disease mucosa is not caused by activated suppressor cells, excessive lymphokine utilization or immune stimulation, a defective response to activation signals, or production of inhibitory substances. Rather, the low interleukin-2 activity appears to be related to a loss of interleukin-2-producing mucosal CD4+ T cells. It is concluded that abnormalities of intestinal CD4+ T-cell function are associated with the immunopathogenesis of Crohn's disease and ulcerative colitis.

Adolescent↗
PubMed1986

Richter's syndrome mimicking chronic colitis. A patient with diffuse histiocytic lymphoma complicating chronic lymphocytic leukemia.

A 62-year-old woman developed diffuse histiocytic lymphoma in the course of chronic lymphocytic leukemia and manifested symptoms mimicking chronic ulcerative colitis. Chronic lymphocytic leukemia may be complicated by the development of lymphoma designated Richter's syndrome. These lymphomas may present in the gastrointestinal tract with signs and symptoms suggestive of chronic inflammatory bowel disease. Initial diagnostic studies, especially barium studies, may yield similar findings. However, histologic findings and clinical course are particularly important in differentiating the disorders.

Antineoplastic Agents↗
PubMed2005

Probiotics ameliorate recurrent Th1-mediated murine colitis by inducing IL-10 and IL-10-dependent TGF-beta-bearing regulatory cells.

Recent studies of murine models of mucosal inflammation suggest that, whereas some kinds of bacterial microflora are inducers of disease, others, known as probiotics, prevent disease. In the present study, we analyzed the regulatory cytokine and cell response to probiotic (VSL#3) administration in the context of the Th1 T cell colitis induced by trinitrobenzene sulfonic acid treatment of SJL/J mice. Daily administration of probiotics for 3 wk to mice during a remission period between a first and second course of colitis induced by trinitrobenzene sulfonic acid, resulted in a milder form of recurrent colitis than observed in mice administered PBS during this same period. This protective effect was attributable to effects on the lamina propria mononuclear cell (LPMC) population, because it could be transferred by LPMC from probiotic-treated mice to naive mice. Probiotic administration was associated with an early increase in the production of IL-10 and an increased number of regulatory CD4+ T cells bearing surface TGF-beta in the form of latency-associated protein (LAP) (LAP+ T cells). The latter were dependent on the IL-10 production because administration of anti-IL-10R mAb blocked their appearance. Finally, the LAP+ T cells were essential to the protective effect of probiotics because administration of anti-IL-10R or anti-TGF-beta at the initiation of recurrent colitis induction or depletion of LAP+ T cells from LPMC abolished the latter's capacity to transfer protection to naive recipients. These studies show that probiotic (VSL#3) administration during a remission period ameliorates the severity of recurrent colitis by inducing an immunoregulatory response involving TGF-beta-bearing regulatory cells.

Adoptive Transfer↗
PubMed2006

CXC chemokine receptor 3 expression increases the disease-inducing potential of CD4+ CD25- T cells in adoptive transfer colitis.

BACKGROUND: CD4CD25 T cells induce severe colitis when injected into immunodeficient recipients. The migration of disease-inducing cells to the bowel is controlled by adhesion molecules and chemotactic proteins. Chemokine receptors expressed on the T cells are therefore potential targets for anti-inflammatory therapy in inflammatory bowel disease. In this study, we have investigated the role of the chemokine receptor CXCR3 in the development of chronic colitis in a murine model. METHOD: Expression of CXCR3 on CD4 T cell from normal and colitic mice was assessed by flow cytometry. Development of colitis was followed after transfer of either normal or CXCR3CD4CD25T cell into immunodeficient host. In addition, the ability of regulatory T cell to function in vivo in the absence of CXCR3 was tested. RESULTS: We find CXCR3 to be expressed on 80% to 90% of CD4 T cells isolated from colitic mice compared with only 4% to 10% of CD4 T cells in normal naïve mice. Injecting CD4CXCR3CD25 T cells into immunodeficient hosts results in an ameliorated form of colitis with a lack of clinical symptoms, suggesting that CXCR3 expression is important for enteroantigen priming of CD4 T cells and/or subsequent migration into the gut wall. In contrast, CXCR3 expression does not affect the function of regulatory T cells because CXCR3 regulatory T cells are just as capable as their wild-type counterpart of controlling disease development. The diminished disease-inducing capability of CXCR3 T cells is not caused by the absence of enteroantigen specificity; we also tested the enteroantigen-specific proliferative ability of CD4CD25 T cells from CXCR3 mice in vitro and found that they respond even more strongly than wild-type cells. CONCLUSIONS: The present data indicate that CXCR3 plays an important role in controlling the migration of disease-inducing CD4CD25 T cells into the gut wall. In contrast, lack of CXCR3 expression by regulatory T cells does not compromise their function in this model of colitis.

Adoptive Transfer↗
PubMed1997

[Immunology in medical practice. IV. Inflammatory bowel diseases: pathogenic starting points for specific therapy].

The cause of inflammatory bowel diseases is unknown, but T-cells play an important part in the pathogenesis of Crohn's disease. It was shown in recent years that activated T-cells produce certain cytokines that cause inflammation (interferon-alpha, tumour necrosis factor-alpha or TNF-alpha), but also cytokines (interleukin-10 or IL-10, transforming growth factor-alpha) which on the contrary inhibit inflammation. On the basis of this knowledge, the mucosal inflammatory reaction can be counteracted in a rational manner: antibodies against TNF-alpha in most patients with Crohn's disease who failed to respond to corticosteroids led to substantial reduction of disease activity. The first experiences with IL-10 treatment of Chrohn patients are also encouraging. It is expected that in the near future still more forms of immunotherapy directed against cytokines will become available.

Animals↗
PubMed1998

A role for NK cells as regulators of CD4+ T cells in a transfer model of colitis.

Previous studies have shown that the chronic inflammation observed in the colon of IL-10-deficient (IL-10(-/-)) mice is mediated by CD4+ Th1 T cells and is dependent on the presence of IFN-gamma for its initial development. As CD4+ T cells from IL-10(-/-) mice will cause colitis when transferred into recombinase-activating gene (Rag)-deficient recipients, we considered the possibility that the recipients' NK cells could be an important source of IFN-gamma for the development of colitis. Therefore, the ability of IL-10(-/-) CD4+ T cells to cause colitis in Rag-deficient recipients that had been depleted of NK cells was tested. Contrary to our expectations, NK cell-depleted recipients of IL-10(-/-) CD4+ T cells developed accelerated disease compared with nondepleted recipients. Furthermore, CD4+ T cells from normal mice (IL-10(+/+)) also caused colitis in NK cell-depleted recipient mice, but not in nondepleted recipients. NK cells inhibited effector CD4+CD45RBhigh T cells, and subsequent experiments showed that this effect was dependent on perforin. Thus NK cells can play an important role in down-regulating Thl-mediated colitis by controlling the responses of effector T cells to gut bacteria.

Adoptive Transfer↗
PubMed1985

Defective generation of tetanus-specific antibody-producing B cells after in vivo immunization of Crohn's disease and ulcerative colitis patients.

In vivo booster immunization with tetanus toxoid normally results in the temporal development of circulating populations of B cells that secrete antibody after in vitro culture. In assessing the humoral immunoregulatory status in patients with inflammatory bowel disease, we found that the antibody production by the B cells that spontaneously secrete tetanus-specific immunoglobulin G in vitro, and which occur in the circulation 7 days postimmunization, was highly variable and below normal in the majority of Crohn's disease and ulcerative colitis patients. The decreased in vitro antibody responses correlated with the lack of an increase in the serum antitetanus immunoglobulin G titers, but did not correlate with disease activity, location, or steroid therapy. The majority of patients who did not produce an immunoglobulin G-antitetanus toxoid antibody response similarly failed to produce an immunoglobulin G-antidiphtheria antibody response after immunization. Lymphocytes from the patients who failed to produce normal levels of antitetanus toxoid antibody did, however, proliferate normally when stimulated by tetanus toxoid in vitro. These results suggest there are in vivo humoral immune defects in inflammatory bowel disease.

Adult↗
PubMed1997

[Cellular immunity in patients with non-specific inflammatory bowel disease for an extended period after surgery].

The study was aimed at investigating the expression of HLA-DR, CD4, CD8, CD56 surface antigens on peripheral blood lymphocytes in patients with non-specific inflammatory bowel diseases in the period of 1-5 years after the surgical procedure. The percentage of rosette forming T-cells in the theophylline test and skin reaction to mycotic and bacterial antigens were assessed simultaneously. The experiment included group of 12 patients (aged 5-55), treated surgically because of Crohn's disease or ulcerative colitis. The lymphocytes' surface antigens were examined by means of monoclonal antibodies and the APAAP procedure. Significantly increased (p < 0.001) percentage of lymphocytes with HLA-DR surface antigens and significantly decreased (p < 0.002) percentage of lymphocytes with CD8 surface antigens were observed in patients with non-specific inflammatory bowel diseases. In 6 of 12 patients the skin test results were negative. The clinical symptoms, which may suggest the maintaining inflammation of the intestinal mucosa were found in 50% of patients examined after surgical procedure because of Crohn's disease. The results suggest there are significant disturbances of cellular immunoreactivity parameters in patients with non-specific inflammatory bowel diseases. It may be one of the causes, which maintain the chronic inflammation of the intestinal mucosa and favour disease recurrence. The cellular immunoreactivity disturbances demonstrated in this study may be the result of the still persisting intestinal mucosa. Inflammation, in spite of deficiency of synonymous clinical symptoms indicating the disease recurrence.

Adolescent↗
PubMed1986

Lymphoglandular complexes of the colon: structure and distribution.

The structure and distribution of lymphoglandular complexes of the colon are described. The cellular composition of these complexes, as detailed by immunohistochemistry and electron microscopy, suggests that they are sites of antigen processing. Variations in structure and in the number of complexes that are found in certain colonic diseases are documented.

B-Lymphocytes↗
PubMed1994

Deficient interleukin 2 dependent proliferation pathway in T lymphocytes from active and inactive ulcerative colitis patients.

There is increasing evidence that ulcerative colitis is associated with an abnormality of the immune system. Although the aetiology remains unknown, it has been suggested that the immune system of these patients is implicated in the pathogenesis of their disease. T cell function was investigated in ulcerative colitis patients and defective phytohaemagglutinin induced T cell mitogenesis was found. The DNA synthesis induced by stimulation with phorbol esters plus ionophore (ionomycin), however, was normal. These changes cannot be ascribed to either decreased interleukin 2 synthesis or to a defective interleukin 2 receptor expression after cellular activation. Moreover, this defective proliferative response of the T lymphocytes was observed even in the presence of saturated concentrations of exogenous interleukin 2. These results emphasise that the interleukin 2 dependent proliferation pathway is deficient in T lymphocytes from ulcerative colitis patients.

Adolescent↗