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PubMed1979

In vitro testing of immunoresponsiveness in patients with inflammatory bowel disease: prevalence and relationship to disease activity immunoresponsiveness in IBD.

Abnormalities in the numbers and function of thymus and function of thymus-derived and bone marrow-derived lymphocytes (T and B cells) and K cells were determined in sixty-nine consecutive patients with Crohn's disease or ulcerative colitis. Rosetting techniques to identify subpopulations of lymphocytes showed a significant decrease in E-rosettes (T cells) and significant increase in EA- and EAC-rosettes (B cells) in patients with inflammatory bowel disease when compared to normals. In vitro lymphocyte transformation responses to mitogens and antigens were depressed to a variable degree. Mean levels of K cell activity were not significantly different from normal controls. A considerable degree of individual variation was noted in all groups. When the results of each groups were considered, none of the laboratory variables correlated with the site, duration or activity of disease, therapy, presence of iron deficiency anemia, weight loss or hypoalbuminaemia. Thus, in vitro evidence of abnormal immune responses in patients with inflammatory bowel disease cannot be directly related to clinical or laboratory variables and probably reflects a multi-factorial aetiology.

Adolescent↗
PubMed1994

Crypt hyperplasia related to increased lymphocyte activation in the rectal mucosa of children with ulcerative colitis.

The presence of cells positive for interleukin-2 receptors (CD25) and the proportion of Ki-67 positive dividing cells in the crypts were studied with monoclonal antibodies using sensitive immunohistochemical techniques in the rectal biopsy specimens taken from 13 children with inflammatory bowel disease (4 Crohn's disease and 9 ulcerative colitis) and 10 controls. In all specimens, but one, from patients CD25+ cells were found in the surface and crypt epithelium, while in none of controls were seen such cells. The mean percentage of dividing crypt cells was significantly higher in ulcerative colitis (36.0%) and in Crohn's disease (34.6%) than in controls (18.4) (p < 0.001 in both comparisons). In ulcerative colitis, a correlation between CD25/CD3 ratios in the surface and crypt epithelium and the percentage of dividing crypt cells was found. We conclude that activated lymphocytes have a role in the crypt hyperplasia of ulcerative colitis.

Adolescent↗
PubMed2002

Abrogated lymphocyte infiltration and lowered CD14 in dextran sulfate induced colitis in mice treated with p65 antisense oligonucleotides.

BACKGROUND AND AIMS: Dextran sulfate sodium (DSS) induced colitis exhibits a predominantly NF-kappaB dependent proinflammatory cytokine profile and shares similarities with human inflammatory bowel disease (IBD). Lamina propria macrophages of IBD patients display elevated levels of NF-kappaB p65. Knowing the role of NF-kappaB in IBD, we investigated the beneficial cellular mechanisms underlying the lasting effect of a single p65 antisense treatment in DSS-colitis mice. METHODS: One local dose of p65 antisense oligonucleotides was administered in DSS colitis mice. Ten days later the mice were killed and examined at cellular and biochemical levels. The level of p65 in lamina propria cells was determined by electrophoretic mobility shift assay and by intracellular immunofluorescent staining of nuclear p65 levels, using laser scanning cytometer. RESULTS: FACS analysis demonstrated a considerable drop in infiltrating lymphocytes and a drastic reduction in CD14+ cells in mice treated with p65 antisense oligonucleotides. Moreover, abrogation of inflammation extended all the way to the cecum in treated mice. Treatment was correlated with decreased DNA binding activity of NF-kappaB. CONCLUSION: Our data strongly support a model in which p65 antisense treatment possesses the capacity to disrupt the pathogenic autocrine loop propagated by NF-kappaB at the chronic phase of IBD.

Animals↗
PubMed1996

Lymphocytic encephalomyeloneuritis as a neurologic complication of ulcerative colitis.

Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease (IBD) showing immunologic abnormalities and association with autoimmune states (Snook et al., 1989). Extraintestinal manifestation of UC affect various organ systems (Podolsky, 1991). We describe morphologically documented encephalomyeloneuritis in a 58-year-old white male with UC in full remission providing support for the concept that ulcerative colitis may be complicated by neurologic manifestations affecting both the central and peripheral nervous system.

Colitis, Ulcerative↗
PubMed1999

[Functional status of intestinal t lymphocytes, regulatory mechanisms, and their variations in the course of Crohn disease and ulcerative colitis].

We analyzed the phenotype, proliferative responsiveness, cytokine production and apoptosis susceptibility of lamina propria lymphocytes to different activation pathways. Lamina propria lymphocytes is a population enriched of activated lymphocytes showing a "memory" phenotype. As opposite to peripheral blood lymphocytes, lamina propria lymphocytes show proliferative hyporesponsiveness when stimulated via TCR/CD3 pathway while proliferative response to the CD2 activation pathway is relatively preserved. Under the latter activation pathway, cytokine production, especially IL-4 and IFN-gamma, is higher than that observed in peripheral lymphocytes. When compared to controls, lamina propria lymphocytes isolated from inflammatory bowel disease (Crohn's disease and ulcerative colitis) show distinctive variation in the cytokine production. In particular, Crohn's disease is characterized by an increased production of IFN-gamma, while in ulcerative colitis an increased production of IL-5 is observable. Among the different regulatory mechanisms contributing to maintain immunological homeostasis we analyzed the susceptibility to apoptosis of lamina propria lymphocytes. We found that CD2-activation pathway is regulated by Fas-mediated apoptosis, which regulates proliferation and cytokine production. In inflammatory bowel disease this apoptosis is defective thus contributing to the chronic inflammation and cytokine dysregulation.

Apoptosis↗
PubMed2006

[Cytotoxic T lymphocyte antigen-4 promoter gene polymorphism is significantly associated with ulcerative colitis].

OBJECTIVE: Inflammatory bowel disease (IBD) is characterized by the T-cell excessive activation of intestinal mucosa. Cytotoxic T-lymphocyte associated antigen 4 (CTLA-4) is a negative regulator of T-lymphocyte activation. The aim of the present study is to investigate the association between CTLA-4 promoter -1722 (T/C), -1661 (A/G) polymorphisms and ulcerative colitis (UC) in Han Chinese, in Hubei province of central China. METHODS: Eighty-seven patients with UC and 116 healthy controls were genotyped for CTLA-4 promoter -1722 and -1661 polymorphisms with a method of polymerase chain reaction based restriction fragment length polymorphism. RESULTS: The frequency of "A/G + G/G" genotype at the -1661 site was statistically higher in UC patients than in healthy controls (34.5% vs 15.5%, P = 0.002, OR = 2.865, 95% CI = 1.467-5.596). The frequency of the G allele at the -1661 site was also significantly higher in UC patients than in the controls (19.0% vs 8.2%, P = 0.002, OR = 2.624, 95% CI = 1.435-4.796). However, the distribution of the genotypes at -1722 site was not significantly different between the UC patients and the controls. CONCLUSION: The G allele of CTLA-4 promoter -1661 polymorphism showed a highly significant association with UC in Han Chinese of the central China.

Adult↗
PubMed1978

In vitro cytotoxic effect of lymphocytes and their extracts in inflammatory bowel diseases. I.

From the sera of 20 patients with ulcerative colitis (U.C.) 10 patients with Crohn's Disease (C.D.) and 10 volunteers, lymphocytes were isolated and extracts of whole lymphocytes (T+B+K) and pure T lymphocytes were prepared. Whole lymphocyte extracts were further fractionated into fraction A containing mainly antibody and fraction B containing mainly membrane-bound receptors. The ability of various lymphocytes and their extracts to lyse allogeneic colonic epithelial cells in vitro was tested with and without the addition of 50 microgram of Common antigen (C.A.) used as a blocking agent. The percentage of cells lysed by whole lymphocytes correlated well with the severity of symptoms of the patients with U.C. Pure T lymphocytes were cytotoxic only in C.D. but not in U.C. Isolated extracts fractions A and B were not cytotoxic in active U.C. except when tested in combination. The addition of the Kunin antigen blocked the effect of lymphocytes from patients with active U.C. The results indicate differences in the mechanism of immunological activity of lymphocytes in U.C. and C.D. and show a direct relation of B lymphocytes and K cells to the cytotoxicity of U.C.

B-Lymphocytes↗
PubMed1995

T lymphocytes and immunoglobulins in small and large intestinal mucosa in children with ulcerative colitis.

In 52 children, aged 4-16 years, with ulcerative colitis, behaviour of A,M,G,E globulins and T lymphocytes in the small and large intestinal mucosa was evaluated. The investigations were performed both in the acute phase and remission of the disease. In the final stage of the disease, numerous plasma cells with intensive reaction to IgA and IgM were found in the stroma, while on the epithelial surface they were less marked. An intensive reaction to IgA was observed in remission. Reaction to T lymphocytes was found in single mononuclear stroma cells both in the acute phase and in remission.

Adolescent↗
PubMed2000

Experimental inflammatory bowel disease--role of T cells.

BACKGROUND: Our experiments were aimed to test: 1. which lymphocyte subpopulations participate in mouse colitis, produced by intrarectal (i.r.) deposition of trinitrobenzene sulphonic acid (TNBSA, TNP hapten); 2. the expression of cell adhesion molecules on lymphocytes draining the site of reaction; 3. the influence of mouse haplotype on the development of colitis. METHODS: CBA/J, BALB/c and C57BI/6 inbred and outbred Swiss Webster strains were used. Mesentheric lymph node (MLN) cells of immunized animals, unseparated or separated into CD4+, CD8+ or gammadelta+ and alphabeta+ T cell subpopulations or depleted of B lymphocytes, were transferred into recipients which were challenged i.r. with TNBSA. Inflammatory reaction in the colon was confirmed macro- and microscopically and by myeloperoxidase (MPO) level. MLN lymphocyte surface markers were tested cytofluorimetrically using appropriate antibodies. RESULTS: Sensitization with TNP results in chronic colitis (hapten dose-dependent colon weight gain and cellular infiltrate, significant increase of MPO level) only in CBA/J and BALB/c strains and can be adoptively transferred in a cell-dose dependent manner into syngeneic recipients by T alphabeta+ cells of both CD4+ and CD8+ subpopulations. T gammadelta+ cells were ineffective and B lymphocytes do not participate in the passive transfer reaction. In MLN the number of T lymphocytes positive for cell adhesion molecules particularly LPAM-1 (V-CAM1) and LPAM-2 increases significantly. CONCLUSIONS: Both CD4+ and CD8+ lymphocytes participate in the development of TNP-induced colitis. High MPO level may suggests that both Th1 and Th2 cells are involved. Colitis is accompanied by a significant accumulation in MLN of T lymphocytes positive for several cell surface adhesion molecules characteristic for memory T cells. Significant differences in susceptibility to develop colitis were found between different strains of mice.

Animals↗
PubMed1999

Impaired mitogenic response of peripheral blood T cells in ulcerative colitis is not due to apoptosis.

An abnormal immune response may play a pathogenic role in ulcerative colitis (UC). Animal models suggest that T-cell regulation may be of central importance in the inflammatory process. Our aims were the characterization of the phenotype and functional status of circulating T-cells in ulcerative colitis patients and to determine if activation-induced cell death in CD4 and CD8 lymphocytes in patients differs from healthy controls. Forty-eight patients (24 women and 24 men) fulfilling the histopathological, clinical, and immunological criteria for UC were studied. T-cell phenotype and function were studied in blood lymphocytes from patients with ulcerative colitis and healthy donors by flow cytometric analysis, as well as [3H]thymidine incorporation. There were no significant differences in the percentage of T-cell subpopulations (CD3, CD4, CD8) and NK cells in the different groups. The percentage of cells in growth phase S+G2M at two and three days of phytohemagglutinin (PHA) stimulation was significantly decreased in UC patients, but the percentage of CD4+ and CD8+ cells in UC patients that showed apoptosis was not significantly different than that in the control group. Proliferative responses to IL-4 also suggested that a reduced responsiveness to this cytokine may be involved in UC. In conclusion, the impaired proliferative response to PHA of T lymphocytes from UC patients is not associated with an in vitro increase in the apoptotic response in CD4+ or CD8+ cells. A reduced IL-4 response may be involved in this peculiar mitogenic response. These changes may be pathogenic or a favorable adaptive mechanism.

Adult↗
PubMed2002

Collagen-binding integrin alpha1beta1 regulates intestinal inflammation in experimental colitis.

Central to inflammatory responses are the integrin-mediated adhesive interactions of cells with their ECM-rich environment. We investigated the role of the collagen-binding integrin alpha(1)beta(1) in intestinal inflammation using the mouse model of colitis induced by dextran sodium sulfate (DSS). mAb's directed against murine alpha(1) were found to significantly attenuate inflammation and injury in DSS-treated wild-type mice; similar protection was seen in mice deficient for alpha(1)beta(1) integrin. Blockade or loss of alpha(1)beta(1) was also associated with decreased mucosal inflammatory cell infiltrate and cytokine production. Importantly, we demonstrated that development and alpha(1)-mediated inhibition of DSS-induced colitis occurred independently of lymphocytes (Rag-2(-/-) mice), and identified the monocyte as a key alpha(1)beta(1)-expressing cell type involved in the development of colitis in this model. In response to DSS, both alpha(1) deficiency and anti-alpha(1) mAb treatment significantly reduced monocyte accumulation and activation within the lamina propria. In summary, the data demonstrate that engagement of leukocyte-associated alpha(1)beta(1) receptors with ECM plays a pivotal role in mediating intestinal inflammation via promotion of monocyte movement and/or activation within the inflamed interstitium. Therapeutic strategies designed to disrupt such interactions may prove beneficial in treating intestinal inflammation.

Animals↗
PubMed1995

Non-lymphoid and lymphoid cells in acute, chronic and relapsing experimental colitis.

In rodents, intracolonic administration of ethanol 30% induces an acute colitis, while administration of 2,4,6-trinitrobenzene sulphonic acid (TNBS) in ethanol induces a longer lasting colitis. In the acute and chronic stages of experimental colitis, lymphoid and non-lymphoid cells were studied in the colon by immunohistochemistry. During the acute inflammation a high damage score of the colon was observed, which was related to an increase in the number of macrophages and granulocytes. Also a change in distributional patterns of macrophage subpopulations was found. The chronic stage of TNBS-ethanol-induced colitis was characterized by an increase in the number of lymphocytes, especially T cells. These data suggest that macrophages and granulocytes are important in the acute phase of experimental colitis, while lymphocytes play a pivotal role in the chronic stage. As most inflammatory bowel disease (IBD) patients have relapses during the chronic disease, we attempted to induce a relapse during experimental colitis by giving a second i.p. or s.c. dose of TNBS. This resulted in increased damage scores of the colon, new areas of ulceration and a further increase in macrophage numbers. No effect on the number of granulocytes was seen. These results indicate that it is possible to mimic relapses in experimental colitis by a second administration of TNBS, and suggest that the rats had been sensitized by the first dose of TNBS, given into the colon.

Acute Disease↗
PubMed2001

MAdCAM mediates lymphocyte-endothelial cell adhesion in a murine model of chronic colitis.

Previous studies have revealed that the expression of several endothelial cell adhesion molecules [e.g., intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and mucosal addressin cell adhesion molecule 1 (MAdCAM-1)] is dramatically elevated in the chronically inflamed colonic vasculature of severe combined immunodeficient (SCID) mice reconstituted with congenic CD4+, CD45RB(high) T lymphocytes. The objective of this study was to define the contribution of different endothelial cell adhesion molecules to the lymphocyte-endothelial cell (L/E) adhesion observed in the colonic microvasculature in this experimental model of inflammatory bowel disease. Fluorescently labeled T lymphocytes, isolated from spleens of normal BALB/C mice, were injected intravenously into SCID mice that had been reconstituted with CD4+, CD45RB(high) T lymphocytes either before (3 wk after reconstitution) or after (7 wk postreconstitution) the onset of clinical signs of colitis (i.e., diarrhea, loss of body wt). Intravital fluorescence microscopy was used to quantify L/E adhesion in different-sized venules of the colonic submucosa during the development of colitis. L/E adhesion was noted in some segments of the vasculature in precolitic SCID mice (3 wk after reconstitution) but not in similar-sized vessels of control (wild type and SCID) mice. L/E adhesion was observed in a greater proportion of venules and occurred with greater intensity in the mucosa of colitic mice (7 wk postreconstitution). Pretreatment with a blocking monoclonal antibody against MAdCAM-1, but not ICAM-1 or VCAM-1, significantly and profoundly reduced L/E adhesion in colitic mice. Immunohistochemical staining also revealed the localization of T cells on colonic endothelial cells expressing MAdCAM-1. These findings indicate that MAdCAM-1 is largely responsible for recruiting T lymphocytes into inflamed colonic tissue.

Animals↗
PubMed2006

Infiltration of CD19+ plasma cells with frequent labeling of Ki-67 in corticosteroid-resistant active ulcerative colitis.

Abnormalities in humoral immunity are implicated in the pathogenesis of ulcerative colitis. However, the detailed mechanisms of B-cell activation in the locale remain unaccounted for. We analyzed ulcerative colitis from the standpoint of lymphocytic expansion in the loco. Intestinal specimens obtained at surgery from 30 patients with ulcerative colitis treated with corticosteroids and 15 with Crohn's disease were analyzed by immunohistochemistry and flow cytometry. Ulcerative colitis was characterized by a diffuse distribution of Ki-67(+) small round cells particularly in the ulcer base (that were CD19(+) and CD20(-)), with a significant number of them also CD138(+). Immunoelectron microscopy for CD19 revealed an abundance of rough endoplasmic reticulum in the cytoplasm. These indicated that they are of immature plasma lineage cells. By contrast, plasma cells in Crohn's disease were negative for CD19, and the labeling for Ki-67 was infrequent, showing mature phenotype. Flow cytometry revealed an occurrence of CD19(+) and CD20(-) cells in ulcerative colitis but not in Crohn's disease. The labeling index of Ki-67 among CD19(+) plasma cells was positively correlated with the clinical activity of ulcerative colitis. High labeling of Ki-67 in CD19(+) plasma cells is specific for active ulcerative colitis that was resistant to medical treatment by corticosteroids.

Adolescent↗
PubMed2001

In-vitro cyclosporin sensitivity of proliferating lymphocytes is predictive of in-vivo therapeutic response in ulcerative colitis.

BACKGROUND: The efficacy of cyclosporin in the management of ulcerative colitis is recognized. Not all patients respond to this treatment. Existing clinical and laboratory parameters are of little use in identifying those most likely to respond. AIMS: To determine whether in-vitro sensitivity to cyclosporin as measured by a lymphocyte proliferation assay is predictive of in-vivo response to therapy. METHODS: The study comprised seven responders with ulcerative colitis, seven non-responders, and 14 healthy matched controls. A lymphocyte proliferation assay was carried out in the presence of a range of concentrations of cyclosporin and a dose-response curve constructed for each subject. The IC(50) value, the concentration of cyclosporin that resulted in 50% inhibition of proliferation, was calculated for each subject. IC(50) values for responders, non-responders and controls were compared using a Mann-Whitney test. RESULTS: There was a wide range of values obtained for the study group as a whole. IC(50) values for non-responders were significantly higher than those of responders (P < 0.05). CONCLUSIONS: There is a population-wide variation of in-vitro sensitivity to cyclosporin. This is reflected in in-vivo sensitivity as measured by clinical response to cyclosporin treatment. Future therapeutic strategies need to address this inherent variability of individual response to therapy.

Adult↗
PubMed2002

Differentiation between ulcerative colitis and Crohn's disease by a quantitative immunohistochemical evaluation of T lymphocytes, neutrophils, histiocytes and mast cells.

Mucosal biopsy criteria has limited validity in terms of discrimination between ulcerative colitis (UC) and Crohn's disease (CD). The aim of this study was to set up quantitative immunohistochemical criteria, with a special focus on inflammatory cell distribution within individual specimens and throughout the large bowel. Quantitative evaluation was performed for the density of CD8+, CD45RO+, neutrophil elastase+, CD68+ and mast cell tryptase+ cells in affected and unaffected mucosa taken from 41 patients with UC and 61 patients with CD. Each slide was examined at the highest and lowest density fields, which were further divided into the upper and deeper half of mucosa. Multiple logistic regression analysis using 51 features as independent variables constructed a predictive equation finding the probability of UC (PUC), and the diagnostic categories were subsequently defined based on a receiver-operating characteristic curve. The analysis disclosed five significant features suggesting UC; these implied intense infiltration of CD8+ and mast cell tryptase+ cells, diffuse infiltration of neutrophil elastase+ and CD68+ cells, and continuous infiltration of CD45RO+ cells. The criteria consisted of three diagnostic categories, 'suggestive of UC (PUC > or = 0.7)', 'indeterminate (0.3 < PUC < 0.7)', and 'suggestive of CD (PUC < or = 0.3)'; the criteria had values for sensitivity and specificity exceeding 95%. The immunohistochemical criteria distinguishing UC from CD may help to confirm the diagnosis in patients with ambiguous endoscopic and histological diagnosis.

Biopsy↗