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PubMed2001

Mycophenolate mofetil reduces tissue damage and inflammation in an experimental model of colitis in rats.

BACKGROUND: Lymphocytes are widely believed to be responsible for persistent intestinal inflammation in inflammatory bowel diseases. Mycophenolate mofetil (MMF) is a potent immunosuppressant that inhibits lymphocyte proliferation and has been shown to be effective in preventing allograft rejection after organ transplantation. The purpose of this study was to assess the modulating effects of MMF on intestinal inflammation in an experimental model of colitis in rats. METHODS: Colitis was induced by rectal instillation of trinitrobenzenesulfonic acid (TNBS) in ethanol in male Sprague-Dawley rats. One group of rats (n = 10) was treated with MMF i.p. (25 mg/kg b.w.) daily for 1 week starting 24 h after induction of colitis. A second group of rats (n = 10) was treated with MMF at the same dose 2 days, I day and 1 h prior to induction of colitis. Control animals (n = 10) received vehicle only. After being killed, colonic tissue was macroscopically evaluated for necrosis and microscopically for ulcerations. Sections were stained and examined for the presence of granulocytes. RESULTS: Administration of MMF after induction of TNBS colitis reduced macroscopic injury by 62% compared to control animals (P = 0.01). Microscopic ulcerations were reduced by 64% compared to controls (P = 0.009). In addition, posttreatment significantly reduced the number of granulocytes. MMF pretreatment did not significantly prevent macroscopic or microscopic tissue damage, or change the number of granulocytes. CONCLUSION: Systemic administration of MMF significantly ameliorates tissue damage in a model of experimental colitis in rats suggesting that this compound may play an important role as an immunosuppressant in the therapy of inflammatory bowel diseases.

Animals↗
PubMed2000

Expression of glucocorticoid receptor beta in lymphocytes of patients with glucocorticoid-resistant ulcerative colitis.

BACKGROUND & AIMS: Recently, the glucocorticoid receptor beta (hGRbeta) was suggested to play a role as a dominant negative regulator for determining glucocorticoid response. The aim of this study was to clarify whether reverse-transcription polymerase chain reaction (RT-PCR) analysis of hGRbeta messenger RNA (mRNA) can predict the response to glucocorticoids in patients with ulcerative colitis. METHODS: Total RNA obtained from peripheral blood mononuclear cells (PBMCs) of 23 patients with ulcerative colitis and 20 healthy volunteers was reverse transcribed; the resulting complementary DNA was amplified using specific primers for hGRalpha and hGRbeta. Protein expression of hGR in PBMCs was confirmed by immunoprecipitation-Western blot analysis. RESULTS: The expression of hGRalpha mRNA (477 base pairs) was detected in all patients and all healthy volunteers. In contrast, a hGRbeta mRNA (366 base pairs) was detected in 1 (9.1%) of 11 glucocorticoid-sensitive patients, 10 (83.3%) of 12 glucocorticoid-resistant patients, and 2 (10%) of 20 healthy volunteers. The positive rate of hGRbeta mRNA in the resistant group was significantly higher than that in the sensitive group (P = 0.0019). The hGRbeta band could be detected by immunoprecipitation-Western blotting in hGRbeta mRNA-positive patients. CONCLUSIONS: The results show that the expression of hGRbeta mRNA in PBMCs examined by RT-PCR may serve as a novel predictor of glucocorticoid response in ulcerative colitis.

Adolescent↗
PubMed1999

Predicting therapeutic outcome in severe ulcerative colitis by measuring in vitro steroid sensitivity of proliferating peripheral blood lymphocytes.

BACKGROUND: Up to 29% of patients with severe ulcerative colitis (UC) fail to respond to steroid treatment and require surgery. Previous studies have failed to show a clear correlation between failure of steroid treatment in severe UC and measures of disease severity. The reasons for treatment failure therefore remain unknown. AIM: To investigate the hypothesis that patients with severe UC who fail to respond to steroid treatment have steroid resistant T lymphocytes. METHODS: Eighteen patients with severe UC were studied. After seven days' treatment with high dose intravenous steroids they were classified as complete responders (CR), incomplete responders (IR), or treatment failures (TF). Within 48 hours of admission blood was taken and the antiproliferative effect of dexamethasone on phytohaemagglutinin stimulated peripheral blood T lymphocytes was measured. Maximum dexamethasone induced inhibition of proliferation (I(max)) was measured. RESULTS: In vitro T lymphocyte steroid sensitivity of TF and IR patients was significantly less than that of CR patients. Both TF and 3/5 IR patients had an I(max) of less than 60%; all CR patients had an I(max) of greater than 60%. No significant correlation was seen between response to treatment and disease severity on admission. When in vitro T lymphocyte steroid sensitivity was remeasured three months later, there was no difference between the groups. CONCLUSIONS: Results suggest that T lymphocyte steroid resistance is an important factor in determining response to steroid treatment in patients with severe UC and may be more predictive of outcome than disease severity.

Adult↗
PubMedDate not supplied

Changes in circulating levels of HIV, CD4, and tissue expression of HIV in a patient with recent-onset ulcerative colitis treated by surgery. Case report.

OBJECTIVE: To determine CD4+ T-cell count and circulating and tissue levels of HIV before and after surgery in a patient with recent-onset ulcerative colitis. STUDY DESIGN/METHODS: CD4 lymphocytes and circulating and tissue HIV RNA levels were measured in an HIV-infected patient with ulcerative colitis before and after proctocolectomy. RESULTS: Approximately 3 weeks prior to surgery for ulcerative colitis that was unresponsive to corticosteroids, the patient's CD4 count was 930 cells/mm3 and fell to 313 cells/mm3 within 10 days; the viral burden was approximately 80,000 RNA copies/mL. Tissue macrophages and lymphocytes in biopsy and resection specimens were shown to express high levels of HIV RNA by in situ hybridization. Five days postoperatively, the patient became asymptomatic and was discharged on tapering prednisone without antiretroviral agents. After surgery, the patient's CD4 count progressively rose, while viral RNA levels precipitously dropped. At 3, 6, and 15 weeks postoperatively, CD4 and viral RNA counts were 622 cells/mm3 and 31,300 RNA copies/mL, 843 cells/mm3 and 11,400 RNA copies/mL, and 747 cells/mm3 and 1500 RNA copies/mL, respectively. CONCLUSIONS: Circulating levels of HIV and CD4+ cells, as well as tissue expression of HIV, apparently can be influenced by localized inflammatory processes such as those occurring in inflammatory bowel disease.

Adult↗
PubMed1978

Studies on the subpopulation and function of peripheral lymphocytes, and lymphocyte reactivity to colonic mucosal antigen and bacterial antigen in patients with ulcerative colitis and Crohn's disease.

Immunological studies were carried out in fifteen cases of ulcerative colitis, three cases of tuberculous colitis, four cases of Crohn's disease and one case of Behcet's disease diagnosed by X-ray, endoscopy or biopsy mainly from the standpoint of cellular immunity. In patients with ulcerative colitis the T-cell population and PHA responsiveness of peripheral lymphocytes were both depressed more than in the control group. At different stages of the disease, the deviation of the values of PHA responsiveness of lymphocytes showed a rather wide range in the active stage and there was also immunological instability. However, when the disease entered remission, the immunological conditions settled down and the pathological condition appeared stable. In contrast to the nonspecific immunological conditions mentioned above, characteristically, there were many examples of a positive lymphocyte response to colonic mucosal and bacterial antigens. In all cases of Crohn's disease the lesions are in the small intestine and there was a reduced response to PHA lymphocytic stimulation which was more pronounced than that in patients with ulcerative colitis. PHA response was also high in tuberculous colitis cases.

Adult↗
PubMed2004

A beta-oxidation-resistant lipoxin A4 analog treats hapten-induced colitis by attenuating inflammation and immune dysfunction.

Lipoxins and aspirin-triggered 15-epi-lipoxins (ATL) are counter-regulatory eicosanoids with potent antiinflammatory actions. Oral efficacy and mechanism of action of ZK-192, a beta-oxidation-resistant 3-oxa-ATL analog, were examined in trinitrobenzenesulphonate (TNBS)-induced colitis. When dosed orally once daily, 300 and 1,000 mug/kg ZK-192 markedly attenuated TNBS colitis in rodents both in preventive and therapeutic regimens. ZK-192 attenuated weight loss, macroscopic and histologic colon injury, mucosal neutrophil infiltration, and colon wall thickening. ZK-192 was as effective as 3-10 mg/kg oral prednisolone. ZK-192 decreased mucosal mRNA levels for several inflammatory mediators: inducible nitric oxide synthase, cyclooxygenase 2, and macrophage inflammatory protein 2. ZK-192 also decreased mucosal mRNA and protein levels of T helper 1 effector cytokines: tumor necrosis factor alpha, IL-2, and IFN-gamma. Systemic levels of these cytokines were also dramatically attenuated. CD3/CD28-mediated costimulation of T helper 1 effector cytokine release in lamina propria mononuclear cells was markedly inhibited by ZK-192 ex vivo and in vitro. ZK-192 also prevented colitis in lymphocyte-deficient severe combined immunodeficient mice, with approximately 75% inhibition of mucosal tumor necrosis factor alpha and IL-2 levels. The results are further evidence that innate immune cells function as triggers for hapten-induced colitis. The combined antiinflammatory and immunomodulatory effects of ZK-192 in TNBS colitis suggest that ATL analogs may be an attractive oral treatment approach for inflammatory bowel diseases.

Animals↗
PubMed1995

Study of cytokines in ulcerative colitis.

We investigated the lymphocyte-activation antigens and the expression of cytokine genes in the mucosa of ulcerative colitis (UC). Fresh colonic mucosal biopsy specimens from patients with UC and controls were fixed for the immunohistochemical study of CD4, HLA-DR, and CD25, and other specimens were prepared for the RNA analysis of cytokines. Gene expression was evaluated by the reverse transcription-polymerase chain reaction, and the radioactivity of dot-blotted amplified cDNA was standardized by co-amplified beta-actin cDNA. The inflamed mucosa of active UC showed increased CD4+DR+ and CD25+ cells in comparison with control subjects. Active UC showed significantly increased mRNA expression of IL-1 beta, IL-2R alpha, IL-6, IL-8, and TNF alpha compared with the controls. We found no significant difference in the mRNA expression for IL-2, IL-4, IL-10, and IFN-gamma between active UC and controls. Increased CD4+DR+ and CD25+ cells in active UC mucosa indicate mucosal CD4(+) T cell activation in the lamina propria, but we did not clarify Th1 or Th2 specific T cell activation from our study of cytokine mRNA expression. The increased mRNA expression for IL-1 beta, IL-6, and TNF alpha in the mucosal lesions of UC indicates that these inflammatory cytokines may play important roles in the pathogenesis of UC.

Biopsy↗
PubMed1983

Pokeweed mitogen stimulated immunoglobulin production by peripheral blood lymphocytes in vitro: evidence for disordered immunoregulation in patients with ulcerative colitis and Crohn's disease.

Production of immunoglobulins (G, A, M) by pokeweed mitogen stimulated peripheral blood lymphocytes was studied in 81 patients with inflammatory bowel disease and compared with 40 patients with mild gastrointestinal disorders (controls). Immunoglobulin production was dependent on the concentration of mononuclear cells in culture, being maximal at the lowest concentration used (2.5 X 10(5)/ml). Adherent monocytes exerted suppression when cultures were reconstituted with more than 20% of these cells. T lymphocyte depleted cells (B cells) demonstrated T cell helper/suppressor dependence for immunoglobulin production in an isotype specific manner, the optimal T cell concentration for 'helper' activity being lowest for IgG and highest for IgM. In patients with active ulcerative colitis (UC) there was a reduction in the T cell concentration for optimal helper activity that was not isotype specific suggesting an increase in non-specific T cell helper activity. T cell helper activity reverted toward control levels in patients with UC in disease remission, except in the case of IgA production where there was a significant diminution of IgA production and of T helper activity for IgA synthesis. Patients with Crohn's disease were distinguished from both UC and control patients by: (1) reduced immunoglobulin production at low lymphocyte concentrations; (2) reduced monocyte-mediated suppression of immunoglobulin production and (3) no shift in T cell concentration for optimal helper activity for IgG and IgA with active disease.

Adult↗
PubMed2003

[Enterocolic phlebitis. Description of a case and review of the literature].

OBJECTIVE: To report about a case of enterocolic phlebitis, a rare cause of ischemic intestinal necrosis. RESULTS AND CONCLUSIONS: The patient, a 71 year-old male, presented with signs of acute abdomen. A right hemicolectomy was performed, which revealed a tubulovillous adenoma with high grade dysplasia located in the ascending colon, and a diffuse ischemic colitis. A localized lymphocytic and granulomatous phlebitis was present in the resected colon. The arteries were spared by the inflammatory process. The patient is alive and well 7 years after surgery. The literature concerning enterocolic phlebitis, a peculiar form of localized intestinal vasculitis, is briefly summarized.

Abdomen, Acute↗
PubMed2001

Collagenous gastritis associated with lymphocytic gastritis and celiac disease.

Collagenous gastritis is a rare disorder, with only 8 cases reported in the literature, 2 in children and 6 in adults. We report an additional case of collagenous gastritis in a 42-year-old man with celiac disease. A thickened (>10 microm) subepithelial collagen band with entrapped capillaries, fibroblasts, and inflammatory cells was seen in the stomach, associated with lymphocytic gastritis. The duodenal mucosa showed severe villous atrophy but no subepithelial collagen deposition. No evidence of lymphocytic or collagenous colitis was found in the colon. The patient became symptom-free on a gluten exclusion diet and showed partial improvement of histopathologic findings after 3 months. Collagenous gastritis is a rare disease, but a wider recognition of its histopathologic features and clinical associations may bring more cases to light and provide additional clues in determining its etiology and pathogenesis.

Adult↗
PubMed1998

Labelling lymphocytes with technetium99m-hexamethyl propyleneamine oxime for scintigraphy: an improved labelling procedure.

Leukocyte scintigraphy has been used as a standard diagnostic procedure for the detection of inflammation in vivo. In this study, we developed a method of labelling purified lymphocytes with technetium99m-hexamethyl propyleneamine oxime (Tc99m-HMPAO) without significantly impairing their function. This was confirmed by measurements of in vitro lymphocyte adhesion and migration and of both necrotic and apoptotic cell death. The results of the in vitro control studies indicate that the dysfunction of leukocytes caused by Tc99m-HMPAO labelling can be minimized by using a gentle labelling method and low Tc99m activity. Because lymphocytes have been thought to participate specifically in the pathogenesis of inflammatory bowel disease (IBD), we compared scintigraphies obtained with Tc99m-HMPAO-labelled purified lymphocytes and mixed leukocytes in colitis patients. We found that a lower number of Tc99m-HMPAO-labelled peripheral blood lymphocytes accumulated in the inflamed colon during the first 4 h than labelled mixed leukocytes. The results are likely to reflect the dissimilar kinetics of lymphocyte traffic compared with granulocytes in IBD. We do not recommend the use of Tc99m-HMPAO-labelled purified lymphocytes as a diagnostic tool in chronic colitis. However, the in vitro data indicate that Tc99m-HMPAO-labelled lymphocytes may be suitable for studying short term lymphocyte recirculation and lymphocyte kinetics in other types of inflammation.

Adolescent↗
PubMed2004

Therapeutic effects of a new lymphocyte homing reagent FTY720 in interleukin-10 gene-deficient mice with colitis.

BACKGROUND: FTY720 is a novel reagent that possesses potent immunosuppressive activity. The immunosuppression induced by FTY720 is mediated by completely different mechanisms from those of conventional immunosuppressants, that is, by altering the tissue distribution of lymphocytes rather than inhibiting activation. In this study, we examined the efficacy of FTY720 in the treatment of chronic colitis in an interleukin-10 gene-deficient (IL-0-/-) mouse model. METHODS: FTY720 was administered orally for 4 weeks to IL-10-/- mice with clinical signs of colitis. The gross and histologic appearance of the colon and the numbers, phenotype, cytokine production, and apoptosis of lymphocytes were compared with those characteristics in a control group. RESULTS: Single-dose administration of FTY720 resulted in the sequestration of circulating lymphocytes within the secondary lymphoid tissues. Four-week administration resulted in a significant reduction of the CD4+ T lymphocytes subpopulation in the colonic lamina propria and IFN-gamma production of the colonic lymphocytes, accompanied by a significant decrease in the severity of colitis. CONCLUSIONS: Treatment of established colitis in IL-10-/- mice with FTY720 ameliorated the colitis, probably as a result of decreasing the number of lymphocytes in the colonic mucosa and an associated reduction in IFN-gamma production.

Animals↗
PubMed2002

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↗
PubMed2001

T-large granular lymphocyte leukemia accompanied by an increase of natural killer cells (CD3-) and associated with ulcerative colitis and autoimmune hepatitis.

Clonal expansion of large granular lymphocyte(LGL) have been classified into T-LGL and NK-LGL leukemia. T-LGL leukemia cells have a CD3+ phenotype and show clonal T-cell receptor(TCR) gene rearrangement. NK-LGL leukemia cells have a CD3- phenotype and no TCR gene rearrangement. We report a case of T-LGL leukemia accompanied by NK LGL expansions in a 65-year-old man who was observed 3 years earlier to have a LGL lymphocytosis in association with ulcerative colitis(UC) and autoimmune hepatitis (AIH). Phenotypic analysis of peripheral blood by flow cytometry disclosed an increase of both T-LGL(CD3+,CD56-,CD57+,and TCRalphabeta+) and NK-LGL (CD3-,CD16+,CD56+, and CD57+). Clonal rearrangement of the TCR beta gene was detected. A diagnosis of UC and AIH was made on the basis of the X-ray and mucosal biopsy findings of the large intestine, and on the scoring system for diagnosis of AIH, respectively. The disease was nonprogressive, and mesalazine and prednisolone were successful for treatment of UC and AIH. Previously reported cases of T-LGL, NK-LGL leukemia, or NK cell lymphocytosis had no association with UC or AIH, and there have been no reports having both T-LGL leukemia with T-cell receptor gene rearrangement and chronic NK cell lymphocytosis co-existing in a single patient.

Anti-Inflammatory Agents↗
PubMed2006

Analysis of cytotoxic T lymphocyte associated antigen 4 gene polymorphisms in patients with ulcerative colitis.

BACKGROUND AND AIM: Ulcerative colitis (UC) is a multifactorial disease associated with dysregulated immunity. Recently, cytotoxic T lymphocyte associated antigen 4 (CTLA-4) gene polymorphisms have been reported in association with several autoimmune diseases in several populations. In the present study, the possible implication of the CTLA-4 gene as a risk factor for UC in the Iranian population was investigated. METHODS: One hundred UC patients and 100 healthy subjects were studied. CTLA-4 exon 1 position 49 (A/G: codon 17: Thr/Ala) polymorphisms were investigated by polymerase chain reaction single strand confirmation polymorphism method. Four of the patients and one of the healthy controls were excluded from the study because of incomplete DNA extraction. RESULTS: The allele frequencies of A and G in 96 patients (A: 66.1%; G: 33.9%) were not significantly different from the 99 control subjects (A: 63.1%; G: 36.9%, P > 0.05). No significant differences in the distribution of genotype frequencies were observed between A + 49G gene polymorphisms and UC in the Iranian population (P > 0.05). CONCLUSION: CTLA-4 polymorphism is not associated with UC in the Iranian population.

Adolescent↗
PubMed2005

Regulatory CD4+CD25+ cells reverse imbalances in the T cell pool of bone marrow transplanted TGepsilon26 mice leading to the prevention of colitis.

BACKGROUND AND AIMS: Erroneous thymic selection of developing T lymphocytes may be responsible for the expansion of self reactive T cells or may contribute to the absence of regulatory T cells important in controlling peripheral inflammatory processes. Colitis in bone marrow (BM) transplanted Tgepsilon26 mice is induced by abnormally activated T cells developing in an aberrant thymic microenvironment. We investigated the protective role of regulatory CD4+CD25+ T cells in this model. METHODS: BM from (C57BL/6 x CBA/J) F1 mice was transplanted into specific pathogen free Tgepsilon26 mice (BM-->Tgepsilon26). Transplanted mice received no cells (control), sorted CD4+CD25+, or CD4+CD25- cells from mesenteric lymph nodes (MLN) of normal mice. MLN cell subsets were analysed using membrane markers. Cytokine secretion of MLN cells was measured using intracellular cytokine staining and cytokine secretion in anti-CD3 stimulated cell cultures. Colitis was measured by histological scores. RESULTS: CD4+CD25+ cells were reduced in the MLNs of BM-->Tgepsilon26 mice. Transfer of regulatory CD4CD4+CD25+ but not of CD4+CD25- cells reduced the number of MLN CD4+ T cells in BM-->Tgepsilon26 recipients and increased the number of MLN CD8+ cells, thereby normalising the CD4+/CD8+ ratio. CD4+CD25+ but not CD4+CD25- cell transfer into BM-->Tgepsilon26 mice reduced the number of tumour necrosis factor alpha+ CD4+ cells and increased the secretion of transforming growth factor beta by MLN cells. Transfer of 3 x 10(5) CD4+CD25+ cells after BM transplantation into Tgepsilon26 mice prevented colitis whereas CD4+CD25- cells had no protective effect. CONCLUSIONS: These results suggest that defective selection or induction of regulatory T cells in the abnormal thymus is responsible for the development of colitis in BM-->Tgepsilon26 mice. Transfer of CD4+CD25+ cells can control intestinal inflammation in BM-->Tgepsilon26 mice by normalising the number and function of the MLN T cell pool.

Animals↗