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PubMed2007

A role of a lymphocyte tryptase, granzyme A, in experimental ulcerative colitis.

In the large-intestinal mucosae of rats orally administered dextran sulfate sodium, which induces an enteritis resembling ulcerative colitis (UC), the activity for granzyme A, a lymphocyte tryptase, increased at an earlier stage than that at which UC markers (growth-regulated gene product/cytokine-induced neutrophil chemoattractant-1 and caspase-3) increased. This suggests involvement of the enzyme in the exacerbation and perpetuation of enteritis.

Animals↗
PubMed2005

Transfer of colitis by Galphai2-deficient T lymphocytes: impact of subpopulations and tissue origin.

To elucidate the potential cell population(s) involved in the induction of colitis in inhibitory G protein Galphai2(-/-) mice, Galphai2-deficient or competent bone marrow or splenic and mesenteric lymph node (MLN) T cells were transferred into immunodeficient mice. The mice were followed up to 23 weeks after transfer, recording changes in body weight. Colitis was graded on hematoxylin and eosin-stained colonic tissue, and production of serum interleukin-18 and colon-derived interferon-gamma was measured using ELISA. After adoptive transfer of Galphai2(-/-) bone marrow, severe colitis developed in irradiated wild type recipients, whereas irradiated Galphai2(-/-) mice increased their life span more than 3 times after transfer of wild type bone marrow, accompanied by significant amelioration of colitis. Neither purified Galphai2(-/-) CD4(+), nor CD8(+) splenic or MLN-derived T cells could induce colitis in recombination-activating gene V(RAG) 2(-/-) recipient mice, whereas transfer of splenic Galphai2(-/-) CD3(+) T cells induced severe colitis. In contrast, transfer of Galphai2(-/-) CD3(+) T cells from the MLN caused only minor histopathological changes in the intestinal mucosa. Finally, serum levels of interleukin-18 and interferon-gamma production from colonic tissue cultures correlated well with disease severity. Our results show that bone marrow transplantation can prolong the life of Galphai2(-/-) mice and ameliorate intestinal inflammation. Splenic CD4(+) or CD8(+) T cells on their own were poor inducers of colitis, whereas the combination of both was highly involved in the induction of intestinal inflammation. Furthermore, we show that the tissue origin of CD3(+) T cells is critical for their potency to induce colitis.

Animals↗
PubMed2001

Immunomodulation of experimental colitis: the role of NK1.1 liver lymphocytes and surrogate antigens--bystander effect.

The imbalance between Th1 pro-inflammatory and Th2 anti-inflammatory cytokine-producing cells plays a major role in the pathogenesis of inflammatory bowel disease (IBD). Induction of oral tolerance to colitis-extracted proteins was previously shown to down-regulate the anti-colon immune response, thereby alleviating experimental colitis. Immune bystander effect and liver-associated lymphocytes expressing the NK1.1 marker (NK1.1(+) LAL) have been suggested as being important in tolerance induction. The aims of the present study were to determine whether oral administration of inflammatory and non-inflammatory colon-extracted proteins of different species can induce peripheral immune tolerance and alleviate experimental colitis; and to examine the role of NK1.1(+) LAL in oral tolerance induction. Colitis was induced in C57/B6 mice by intracolonic instillation of trinitrobenzene sulphonic acid (TNBS). Mice received six oral doses of colonic proteins extracted from TNBS-colitis colonic wall, or normal colonic wall, from four different species. Standard clinical, macroscopic, and microscopic scores were used for colitis assessment. Serum interferon gamma (IFNgamma) and interleukin 10 (IL10) levels were measured by ELISA. To evaluate the role of NK1.1(+) LAL in maintaining the balance between immunogenic and tolerogenic subsets of cells, their cytotoxicity functions were tested in tolerized and non-tolerized-mice. The administration of mouse-derived colitis-extracted proteins, or of surrogate proteins extracted from normal mouse colon, or from rat or human inflammatory colons, was found to alleviate experimental colitis. Tolerized mice had less diarrhoea; showed a marked reduction of colonic ulceration, intestinal and peritoneal adhesions, wall thickness, and oedema; and demonstrated a significant improvement of all microscopic parameters for colitis. Induction of tolerance led to an increase in IL10 and a decrease in IFNgamma serum levels. NK1.1(+) LAL cytotoxicity function increased markedly in tolerized mice. In contrast, mice fed with proteins extracted from normal rat, rabbit, and human colon, or from rabbit inflammatory colon, developed severe colitis, with a marked increase in IFNgamma and a decrease in IL10 serum levels, and down-regulation of NK1.1(+) LAL function. This study has shown that oral tolerance can be induced in experimental colitis by means of the feeding of surrogate antigens; this alleviates experimental colitis. NK1.1(+) LAL cytotoxicity function is associated with peripheral tolerance induction and may help to maintain the Th1/Th2 immune balance.

Animals↗
PubMed1988

[Analysis of different lymphocyte subpopulations in patients with nonspecific ulcerative colitis].

A complex of methods based on a rosette forming reaction, was used to study the content of different lymphocytic populations in the peripheral blood of persons with nonspecific ulcerative colitis. Imbalance in the system of immunocompetent cells was shown to develop in this disease: a decrease in the amount of suppressors (T gamma and theophylline sensitive lymphocytes) and a increase in the amount of immature postthymic cells: cells forming rosettes with autologous erythrocytes, and theophylline dependent lymphocytes.

Adolescent↗
PubMed2002

Prevention of colitis by interleukin 10-transduced T lymphocytes in the SCID mice transfer model.

BACKGROUND & AIMS: Regulatory CD4(+) cells secreting the anti-inflammatory cytokine interleukin (IL)-10 play a key role in maintaining the immune balance in the intestinal mucosa. In this study we engineered primary CD4(+) cells to express IL-10 and investigated the efficacy of this approach in offering protection against experimental colitis. METHODS: Spleen-derived CD4(+) cells were transduced by using a retroviral vector to simultaneously express IL-10 and green fluorescent protein (GFP). The therapeutic benefit of CD4(+) cells transduced with IL-10 GFP was studied in experimental colitis, induced by transfer of CD45RB(high) CD4(+) cells to severe combined immunodeficient mice, and in acute trinitrobenzene sulfonic acid (TNBS)-induced colitis. RESULTS: Transferred engineered GFP fluorescent cells were detected for at least 15 weeks in peripheral blood, spleens, colon, and lymph nodes draining the intestine of recipient SCID mice. IL-10-GFP CD4(+) cells prevented CD45RB(high)-induced transfer colitis effectively, whereas no effect was observed after transfer of nontransduced CD4(+) cells. IL-10-GFP CD45RB(high) CD4(+) cells lost the capacity to induce colitis. By contrast, no therapeutic benefit was observed in TNBS-induced colitis. CONCLUSIONS: Primary murine CD4(+) cells that were engineered to express IL-10 by retroviral transduction act as regulatory cells in CD45RB(high)-induced transfer colitis. This approach may induce long-term maintenance of mucosal immune homeostasis in Crohn's disease.

Animals↗
PubMed1988

T lymphocyte subpopulations and immunoglobulin-containing cells in the colonic mucosa of ulcerative colitis; a morphometric and immunohistochemical study.

T lymphocyte subpopulations and immunoglobulin containing cells in the colonic mucosa of 25 patients with ulcerative colitis have been studied using an indirect immunoperoxidase technique. In ulcerative colitis a marked increase in the population of Leu 3a positive cells (helper/inducer T cells) and IgG containing cells was observed in the mucosal lamina propria. In the intraepithelial spaces, a remarkable decrease in the population of Leu 2a positive cells (suppressor/cytotoxic T cells) and a marked increase in the number of Leu 3a positive cells were revealed. There was a very significant correlation between the population of IgG containing cells and the ratio of Leu 3a positive cells to Leu 2a positive cells in the lamina propria of patients with ulcerative colitis. These results suggest that an imbalance of mucosal immunoregulatory T cells and an increased production of IgG occurred in correlation with inflammatory activities of ulcerative colitis.

Adolescent↗
PubMed2005

Lymphocyte telomere dynamics and telomerase activity in inflammatory bowel disease: effect of drugs and smoking.

BACKGROUND: The chromosome instability observed in peripheral blood lymphocytes in ulcerative colitis could be a biomarker of cancer susceptibility. AIM: To determine whether accelerated telomere shortening could explain chromosome instability and assess the effect of drugs and smoking on telomere dynamics in these cells. METHODS: Peripheral blood lymphocytes were isolated from ulcerative colitis, Crohn's disease and non-inflammatory bowel disease control patients. Telomere lengths were measured by quantitative real-time polymerase chain reaction. After activation and cell separation, telomerase activity and human telomerase reverse transcriptase messenger ribonucleic acid were measured by telomerase repeat amplification protocol enzyme-linked immunosorbent serological assay and quantitative real-time polymerase chain reaction, respectively. RESULTS: Age-related telomere loss in peripheral blood lymphocytes was similar in ulcerative colitis, Crohn's disease and control patients. Telomerase activity decreased with age in all groups and correlated positively with telomere length (r = 0.489, P = 0.006). Among Crohn's disease patients, azathioprine was associated with decreased telomerase activity (0.66 vs. 1.54, P = 0.026, P < 0.05) and smoking was associated with decreased human telomerase reverse transcriptase mRNA expression (10.5 vs. 33.3, P = 0.036, P < 0.05). CONCLUSIONS: Telomere shortening is not accelerated and therefore cannot be the cause of the chromosome instability observed in ulcerative colitis peripheral blood lymphocytes. Azathioprine and cigarette smoking modify telomerase expression in these cells.

Adult↗
PubMed1987

Differences in the immunoglobulin synthesis by peripheral blood lymphocytes in Crohn's disease and ulcerative colitis.

To determine whether patients with Crohn's disease and ulcerative colitis differ in their capacity to produce immunoglobulins, we have studied the in vitro immunoglobulin synthesis by peripheral blood lymphocytes of such patients and compared the results with those of healthy controls. The spontaneous immunoglobulin production by peripheral blood lymphocytes from Crohn's disease patients was significantly increased for both IgA and IgG, whereas for IgM the increase did not reach statistical significance. In ulcerative colitis, however, the spontaneous IgA and IgG production was almost identical to that of the healthy controls and thus lower than in Crohn's disease. Pokeweed mitogen stimulation resulted in a significantly enhanced immunoglobulin production in Crohn's disease and in controls, whereas peripheral blood lymphocytes from ulcerative colitis patients were found to be rather insensitive to pokeweed mitogen stimulation. Suppression of the stimulated immunoglobulin production by concanavalin A revealed considerable reduction in all groups studied. In general, the highest suppression was found in patients with Crohn's disease. In patients with Crohn's disease or ulcerative colitis there was no relation between the changes in the in vitro immunoglobulin synthesis and the population of B or T lymphocytes and monocytes present in the peripheral blood. The differences in the spontaneous and stimulated immunoglobulin synthesis by peripheral blood lymphocytes, as found in this study, point to major changes in the regulation of the immunoglobulin synthesis in Crohn's disease and ulcerative colitis.

Adult↗
PubMed1999

Lymphocytic venulitis: an unusual association with microscopic colitis.

A 79 year old man presented with occult gastrointestinal bleeds and anaemia for two years. He had received 40 units of blood over a period of one year, following which he had a subtotal colectomy as no definite cause of the bleeding was apparent. Macroscopically the colon appeared unremarkable. Light microscopy showed prominent lymphocytic venulitis in the proximal portion, gradually merging into lymphocytic and collagenous colitis distally.

Aged↗
PubMed2001

Proteinase-activated receptor 2 is an anti-inflammatory signal for colonic lamina propria lymphocytes in a mouse model of colitis.

The proteinase-activated receptor 2 (PAR-2) is a member of a family of G protein-coupled receptors for proteases. Proteases cleave PARs within the extracellular N-terminal domains to expose tethered ligands that bind to and activate the cleaved receptors. PAR-2 is highly expressed in colon in epithelial and neuronal elements. In this study we show that PAR-2 activation prevents the development and induces healing of T helper cell type 1-mediated experimental colitis induced by intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in mice. A role for PAR-2 in the protection against colon inflammation was explored by the use of SLIGRL-NH(2), a synthetic peptide that corresponds to the mouse tethered ligand exposed after PAR-2 cleavage. TNBS-induced colitis was dose-dependently reduced by the administration of SLIGRL-NH(2), whereas the scramble control peptide, LSIGRL-NH(2), was uneffective. This beneficial effect was reflected by increased survival rates, improvement of macroscopic and histologic scores, decrease in mucosal content of T helper cell type 1 cytokines, protein, and mRNA, and a diminished myeloperoxidase activity. SLIGRL-NH(2), but not the scramble peptide, directly inhibited IFN-gamma secretion and CD44 expression on lamina propria T lymphocytes. Protection exerted by PAR-2 in TNBS-treated mice was reverted by injecting mice with a truncated form of calcitonin gene-related peptide and by sensory neurons ablation with the neurotoxin capsaicin. Collectively, these studies show that PAR-2 is an anti-inflammatory receptor in the colon and suggest that PAR-2 ligands might be effective in the treatment of inflammatory bowel diseases.

Animals↗
PubMed2003

Changes of CD8+CD28- T regulatory cells in rat model of colitis induced by 2,4-dinitrofluorobenzene.

AIM: To determine the changes of CD8+ T subsets especially CD8+CD28- T regulatory cells in rat model of experimental colitis induced by 2,4-dinitrofluorobenzene (DNFB). METHODS: The rat model of experimental colitis was induced by enema with DNFB. Ten days later, colonic intraepithelial and splenic lymphocytes were isolated from colitis animals (n=16) and controls (n=8). The proportion of CD8+ T cells, CD8+CD28+ T cells and CD8+CD28- T regulatory cells were determined by flow cytometry. RESULTS: The model of experimental colitis was successfully established by DNFB that was demonstrated by bloody diarrhea, weight loss and colonic histopathology. The proportion of CD8+ T cells in either splenic or colonic intraepithelial lymphocytes was not significantly different between colitis animals and controls (spleen: 34.6+/-7.24% vs 33.5+/-9.41%, colon: 14.0+/-8.93% vs 18.0+/-4.06%, P>0.05). But CD8+CD28- T regulatory cells from colitis animals were significantly more than those from controls (spleen: 11.3+/-2.26% vs 5.64+/-1.01%, colon: 6.50+/-5.37% vs 1.07+/-0.65%, P<0.05). In contrast, CD8+CD28+ T cells from colitis animals were less than those from controls (spleen: 23.3+/-6.14% vs 27.8+/-9.70%, P=0.06; colon: 7.52+/-4.18% vs 16.9+/-4.07%, P<0.05). The proportion of CD8+CD28- T regulatory cells in splenic and colon intraepithelial CD8+ T cells from colitis animals was higher than that from controls (spleen: 33.3+/-5.49% vs 18.4+/-7.26%, colon: 46.0+/-14.3% vs 6.10+/-3.72%, P<0.005). CONCLUSION: Experimental colitis of rats can be induced by DNFB with simplicity and good reproducibility. The proportion of CD8+CD28- T regulatory cells in rats with experimental colitis is increased, which may be associated with the pathogenesis of colitis.

Animals↗
PubMed1985

Lymphocyte response to a bovine milk protein in ulcerative colitis.

A recently described in vitro test for cow's milk protein hypersensitivity was applied to adult patients with ulcerative colitis. The test system involved the culture of their peripheral blood lymphocytes with and without beta-lactoglobulin, and the results were expressed as a stimulation index. Stimulation with beta-lactoglobulin was significantly higher (P less than 0.02) in patients with active disease than in those with inactive disease or in healthy controls. beta-Lactoglobulin was the only one of four cow's milk proteins that showed this effect. It is concluded that the cow's milk protein beta-lactoglobulin has a specific blastogenic effect on the lymphocytes of patients with active ulcerative colitis, and, therefore, may serve as a marker of disease activity.

Adolescent↗
PubMed2001

No evidence of persistent mumps virus infection in inflammatory bowel disease.

BACKGROUND AND AIM: There is controversy regarding whether paramyxovirus infection is causally associated with inflammatory bowel disease (IBD). The latest cohort study claimed that atypical measles and mumps infections in childhood may be risk factors for later IBD. This study was conducted to clarify the validity of a causal link between persistent mumps virus infection and IBD. SUBJECTS AND METHODS: (1) Amplification of the mumps virus genome was performed in both intestinal specimens (ulcerative colitis 15, Crohn's disease 15, control 10) and peripheral blood lymphocytes (PBL) (ulcerative colitis seven, Crohn's disease six, control three) by reverse transcription-polymerase chain reaction (RT-PCR) followed by Southern hybridisation using primers specific to the viral genome encoding phosphoprotein or haemagglutinin-neuraminidase. (2) Titre of serum antimumps IgG was measured in 16 patients with ulcerative colitis, in 16 patients with Crohn's disease, and in 16 normal controls using an enzyme linked immunosorbent assay. RESULTS: (1) The mumps virus genome was not detected by RT-PCR in intestinal specimens or PBL in any case. (2) Antimumps IgG titre was positive in 7/16 ulcerative colitis, 10/16 Crohn's disease, and 11/16 control specimens. The mean (SEM) titre of antimumps IgG was 12.281 (7.831) in ulcerative colitis, 7.675 (1.608) in Crohn's disease, and 8.637 (1.969) in controls, with no significant difference between the three groups. CONCLUSION: We could not find any evidence to support a causal link between persistent mumps virus infection and IBD.

Adolescent↗
PubMed2006

TH1/TH2-mediated colitis induced by adoptive transfer of CD4+CD45RBhigh T lymphocytes into nude mice.

BACKGROUND: Transfer of CD4CD45RB T cells from normal donors to SCID/Rag-1, 2-deficient mice, which lack T and B cells, leads to the development of a TH1-mediated inflammatory bowel disease (IBD)-like syndrome characterized by extensive mononuclear cell infiltrates and epithelial cell hyperplasia. Because it is well known that B cells are also involved in a multitude of mechanistic pathways in human IBD, this study attempts to establish a new model of colitis in nude mice. METHODS: We transferred CD4CD45RB T cells into athymic nude mice, which lack thymus-dependent T cells but retain normal B cells, to establish and investigate a B cell-involving chronic colitis model. As a control, CD4CD25 T cells were also used. RESULTS: Mice reconstituted with CD4CD45RB but not CD4CD25 T cells developed a wasting disease, with severe infiltrates of B cell aggregates as well as T cells, macrophages, and dendritic cells into the colon and elevated levels of interferon-gamma, tumor necrosis factor-alpha, interleukin (IL)-4, IL-5, and IL-10, by 7 weeks after T cell transfer. Furthermore, the infiltrated lamina propria B cells in colitic nude mice consisted predominantly of massive aggregated immunoglobulin (Ig) M- and scattered IgG-positive cells, but not IgA-positive cells. In contrast, mice reconstituted with CD4CD45RB and CD4CD45RB did not develop wasting disease or colitis. CONCLUSIONS: Collectively, the power of the colitis model induced by the adoptive transfer of CD4CD45RB T cells into nude mice is that one can investigate the roles of TH2-type cells and B cells in a regulatory T cell-depleted condition.

Adoptive Transfer↗