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PubMed1989

[The ratio of various lymphocyte populations in bacillary dysentery and nonspecific ulcerative colitis].

The comparative study of the content of different lymphocyte populations of the peripheral blood in pathological states accompanied by lesions of the mucous membrane of the large intestine has been made. In shigellosis patients the accumulation of lymphocytes having the signs of young post-thymic forms (theophylline-dependent populations) and functionally active forms (Ea-rosette-forming cells) occurs in the circulating blood. In unspecific ulcerous colitis only an increase in the number of immature lymphocytes (theophylline-dependent lymphocytes and autorosette-forming cells) is observed. In both pathological states an increase in the number of O-lymphocytes with Fc gamma-receptors occurs in the circulation blood.

B-Lymphocytes↗
PubMed1993

[An evaluation of the efficacy of different methods for identifying peripheral blood T- and B-lymphocytes in patients with nonspecific ulcerative colitis].

Rosette-forming with sheep's erythrocytes (EAC-RF) and monoclonal antibodies (MCA) were used for account of cell populations and subpopulations in patients with ulcerative colitis and Crohn's disease. It was established that MCA technique does increase accuracy of quantitative determination of immunocompetent cells in such patients but on the whole EAC-RF which is at present more accessible method can be considered quite acceptable for estimation of immune reactivity in nonspecific inflammatory diseases of the colon.

Antibodies, Monoclonal↗
PubMed1979

[Cell-mediated and humoral immunity in ulcerative colitis. Acute phase reactants (author's transl)].

Many findings suggest that the alterations in immune response observed in intestinal inflammatory diseases may play a part in their pathogenesis. This observation led us to study 22 patients with chronic ulcerative colitis, of whom seven were in the acute stage and the other 15 were asymptomatic. The T and B lymphocyte populations were determined as well as the serum levels of immunoglobulins and acid alpha-1-glycoprotein as acute phase reactants. The results were compared with those obtained from a control group of 10 normal individuals. No statistically significant differences were observed in the percentages and absolute values of T and B lymphocytes as compared with the controls. nor in relation to the activity of the lesions. Neither were there any observable variations in the serum concentrations of immunoglobulins. On the other hand, analysis of the acid alpha-1-glycoprotein showed highly significant values as related to the degree of activity of the inflammatory lesion (p less than 0.005). Our results confirmed the value of determining serum acid alpha-1-glycoprotein levels as an index of inflammatory activity. The immunitary parameters under study did not vary in the different stages of the disease.

Adult↗
PubMed1975

The in-vitro action of lymphocytes on autologous colon epithelial cells in ulcerative colitis.

The action in culture of peripheral blood lymphocytes on autologous large-intestinal epithelial cells was studied in 13 patients with severe mucosal ulcerative colitis. Two different methods were used to measure lymphocyte activity. These showed that autologous-lymphocyte-induced release of isotopic label and detachment in monolayer culture of large-intestinal epithelial cells was increased in acute ulcerative colitis when compared with findings in the same studies in six normal subjects. Subsequently in four of the six patients who responded to cortisone it was shown that lymphocyte activity against epithelial cells returned to the normal range. Further control studies showed little lymphocyte activity against autologous skin and ileum, suggesting that autologous-lymphocyte-induced damage of large-intestinal epithelial cells is a tissue-specific reaction in patients with acute ulcerative colitis. The absence of reactivity in other colonic inflammatory diseases also suggested that such increased in vitro lymphocyte activity is disease-specific for ulcerative colitis.

Adolescent↗
PubMed1998

Expression of selectin-binding epitopes and cytokines by CD4+ T cells repopulating scid mice with colitis.

Recruitment into the gut of CD4+ T cells and their activation in the colonic lamina propria (LP) are key events in the development of colitis in scid mice reconstituted with CD4+ T cells from immunocompetent, congenic donor mice. This study investigated the expression of cytokines and selectin-binding epitopes by CD4+ T cells repopulating different tissues of the adoptive scid host. Cells from the inflamed colonic LP of transplanted scid mice produced high amounts of IL-12, IFN-gamma and TNF-alpha but only low amounts IL-4 and IL-10. Intracellular cytokine staining confirmed the presence of large numbers of IFN-gamma- and TNF-alpha-producing effector CD4+ T cells in the colonic LP of scid mice with colitis but also in non-inflamed tissues [spleen (S), peritoneal cavity (PC) and mesenteric lymph nodes (mLN)] of the adoptive host. Cells from these tissues furthermore produced large amounts of IL-12. Ligands for endothelial selectins are involved in recruiting T cells into inflamed tissues. We have analyzed the expression of selectin-binding epitopes on CD4+ T cells repopulating different tissues of the adoptive scid host. We found that a large fraction of CD4+ T cells from inflamed colonic LP and from non-inflamed PC, mLN and S expressed high levels of P- and E-selectin-binding epitopes (P-Lhi) in transplanted scid mice, but not in congenic, immunocompetent control mice. Although P-Lhi CD4+ T cells were enriched in IFN-gamma-producing subsets from most (but not all) tissues, we also found large numbers of in vivo generated P-Llo CD4+ T cells producing pro-inflammatory cytokines. This was in contrast to in vitro generated Th1 CD4+ T blasts that were almost exclusively P-Lhi. In this mouse model, production of Th1-type pro-inflammatory cytokines and expression of surface epitopes binding endothelial selectins are hence strikingly up-regulated in CD4+ T cells residing in inflamed and non-inflamed tissues during the development of colitis.

Animals↗
PubMed1988

T-cell immunoregulation in patients with inflammatory bowel disease. II. Enhanced suppressor T-cell activity in ulcerative colitis.

In a recent study, we have shown that peripheral blood B cells from patients with ulcerative colitis (UC) synthesized less immunoglobulin (Ig) in co-culture with autologous T cells than normal adults' B cells. When UC patients' T cells were co-cultured with normal adults' B cells, Ig synthesis was significantly decreased as compared with normal controls. In contrast, Crohn's disease (CD) patients' B and T cells functioned normally. In the present study, the activity of suppressor T cells in patients with UC and CD was determined. Peripheral blood B and T cells with monocytes were obtained from patients and normal adults of the same age and sex, and co-cultured for 10 days with pokeweed mitogen (PWM). Suppressor T-cell function was measured in mixed co-culture assays in which graded numbers of normal or patient's T cells were added to normal adults' B and T cells with PWM. Immunoglobulins (Ig) M, G and A were measured in culture supernatants using a sensitive enzyme-linked immunosorbent assay. The quantity of Ig present in the culture supernatants was determined from a standard curve. T cells from UC patients significantly decreased immunoglobulin production by control B and T cells (IgM and IgA, p = 0.02; IgG, p = 0.01). In contrast, addition of T cells from CD patients produced no significant differences. Complement mediated, monoclonal OKT8 antibody directed cell lysis revealed that the inhibition observed with UC patients' T cells in co-culture was due to a T8+ suppressor T cell. The degree of inhibition of immunoglobulin synthesis did not correlate with disease activity, duration of illness, location of disease, or corticosteroid treatment. Thus, patients with ulcerative colitis display enhanced suppressor T-cell activity in peripheral blood while patients with CD show normal helper and suppressor T-cell functions. These results provide evidence supporting a role for altered immunoregulatory activity in the pathogenesis of ulcerative colitis.

Adult↗
PubMed2006

Characterization of tumour-infiltrating lymphocytes and apoptosis in colitis-associated neoplasia: comparison with sporadic colorectal cancer.

The development of colorectal cancer is a major complication for patients with chronic idiopathic colitis. Colitis-associated tumours tend to occur at a younger age and be more aggressive than sporadic colorectal cancers. While we have previously associated the presence of tumour-infiltrating lymphocytes (TILs) and increased apoptosis in sporadic colorectal cancer with high-level microsatellite instability and improved prognosis, little is known of the relationship between these variables in colitis-associated colorectal cancer. The aim of this study was to correlate TILs and tumour cell apoptosis in colitis-associated neoplasms stratified according to microsatellite instability. Twenty tumour and 11 dysplastic samples resected from 21 patients with long-standing colitis were analysed for microsatellite instability at 10 microsatellite markers. TIL distribution (CD3, CD8) and function (granzyme B) were quantified by immunohistochemistry. Neoplastic cell apoptosis was assessed using the M30 CytoDEATH antibody. These findings were compared with 40 microsatellite stable (MSS) sporadic colorectal cancers previously evaluated for TILs and neoplastic apoptosis. Low-level microsatellite instability was found in 1/20 colitis-associated tumours. All other colitis-associated lesions were designated MSS. CD3(+) and CD8(+) TIL counts were significantly higher in colitis-associated lesions compared with MSS sporadic colorectal cancer (p < 0.0001, p = 0.001 respectively). Despite their higher TIL density, colitis-associated tumours were more likely to present late (Dukes' stage C or D) (p = 0.02). Functionally, colitis-associated TILs demonstrated significantly less granzyme B expression compared to sporadic cancers (p = 0.002). The level of tumour cell apoptosis was similar between the two groups (sporadic, 1.53%; colitis cancers, 1.45%). In conclusion, MSS colitis-associated tumours have a higher prevalence of CD3(+)/CD8(+) TILs but no associated increase in tumour cell killing by apoptosis. Unlike cytotoxic T cells in sporadic colorectal cancer, TILs do not appear to enhance the prognosis of colitis-associated colorectal cancer. This may be related to an impairment of granzyme B expression within these lesions.

Aged↗
PubMed1991

Active idiopathic ulcerative colitis in a patient with ongoing HIV-related immunodepression.

It is suspected that immune mechanisms are important in the pathogenesis of ulcerative colitis. The following is a case report of a patient with human immunodeficiency virus-related immunodeficiency whose ulcerative colitis ran a course independent of the depression of his peripheral CD4 cells. Thus, peripheral CD4 cells may have little role in the pathogenesis of ulcerative colitis.

Adult↗
PubMed1980

Lymphocyte subpopulations of intestinal mucosa in inflammatory bowel disease.

Lymphocyte subpopulations in peripheral blood (PBL) and intestinal mucosa (IML) of 10 patients with inflammatory bowel disease (IBD) were compared with those of 11 non-IBD controls. PBL were separated on Ficoll/hypaque gradients, and IML were isolated by incubation in dithiothreitol, EDTA, and collagenase. These methods yielded cells of good viability and with intact HLA A and B-antigens. T-cells, identified by neuraminidase-treated sheep RBC rosettes and non-specific esterase staining, comprised approximately 91% of the IML from normal mucosa of all groups. B-cells, identified by erythrocyte-antibody-complement rosettes and surface immunoglobulins, were only 7% of these IML populations. Cell yields were two-fold or more greater from abnormal IBD mucosa, with T-cells ranging from 55 to 95% and B-cells from 2 to 36%. The percentage of Fc receptor bearing cells was low in all specimens. By these methods, T-lymphocytes predominated in intestinal mucosa of both IBD and non-IBD patients, but there is marked increase in the percentage of B-cells isolated from abnormal mucosa in IBD.

Adult↗
PubMed2000

Immunoglobulin leakiness in scid mice with CD4(+) T-cell-induced chronic colitis.

Inflammatory bowel disease in scid mice is initiated by transplantation of CD4(+) T-cells from immunocompetent syngenic donor mice. As the disease progresses, immunoglobulin (Ig)-containing cells appear in the gut lamina propria, suggesting that locally accumulating Ig may play a role in disease development. In the present work we have investigated the relationship between disease progression and patterns or levels of Ig isotypes in the feces of scid mice suffering from an ongoing colitis. The data clearly showed that the severity or progression of the disease did not influence the levels of IgA, IgG1, IgG2a, IgG2b, and IgG3, whereas the level of fecal IgM increased during the course of colitis. The presence of the serum protein alpha-1-antitrypsin in fecal extracts from diseased mice suggests that some of the fecal Ig has leaked through the inflamed epithelial membrane into the gut lumen. Finally, Ig-containing cells were observed in mesenteric lymph nodes and in the spleen, suggesting that the fecal Ig is produced both systemically and locally in the gut wall. In conclusion, the present results demonstrate that the level of IgM increases as colitis progresses. Also, the five remaining major Ig isotypes are increased in the gut lumen of scid mice with colitis, but the individual Ig types vary randomly during the course of the disease. Thus, it is unlikely that immunoglobulins are involved in the immunopathogenesis of this model of colitis.

Animals↗
PubMed2005

Fumigaclavine C, an fungal metabolite, improves experimental colitis in mice via downregulating Th1 cytokine production and matrix metalloproteinase activity.

In the present paper, the effect of Fumigaclavine C, a fungal metabolite, on experimental colitis was examined. Fumigaclavine C, when administered intraperitoneally once a day, significantly reduced the weight loss and mortality rate of mice with experimental colitis induced by intrarectally injection of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS). This compound also markedly alleviated the macroscopic and microscopic appearances of colitis. Furthermore, Fumigaclavine C, given both in vivo and in vitro, showed a marked inhibition on the expression of several inflammatory cytokines, including IL-1beta, IL-2, IL-12alpha, IFN-gamma, TNF-alpha as well as MMP-9 in sacral lymph node cells, colonic patch lymphocytes and colitis tissues from the TNBS colitis mice. Meanwhile, the compound caused a dose-dependent reduction in IL-2 and IFN-gamma from the lymphocytes at the protein level and MMP-9 activity. These results suggest that Fumigaclavine C may alleviate experimental colitis mainly via down-regulating the production of Th1 cytokines and the activity of matrix metalloproteinase.

Acremonium↗