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PubMed1977

Autoantibodies to B lymphocytes in a patient with hypoimmunoglobulinemia. Characterization and pathogenic role.

In a young woman with ulcerative colitis, hypoimmunoglobulinemia, and humoral immunodeficiency, lymphocyte counts vary between 600 and 1,000 per mm(3) with 0.5-1.5% bone marrow-derived (B) cells and 98-99% thymus-derived (T) cells. Anti-lymphocyte antibodies were detected by immunofluorescence and by microlymphocytotoxicity with increased reactivity at +4 degrees C. They belonged to the IgM class and were polyclonal. Studies performed with various normal lymphocyte subpopulations, several lymphoblastoid cell lines and lymphocytes from immunodeficiency patients showed that these antibodies reacted with B cells. The corresponding antigen(s) is distinct from membrane-bound immunoglobulins, is not an alloantigen, and is probably unrelated to the la-like molecules. Pokeweed mitogen stimulated B cells appear to lose this antigen. Cells from various lymphoproliferative disorders were tested. T-derived and "non T-non-B" leukemic cells did not react with the antibody. Malignant cells from B-derived lymphomas and prolymphocytic leukemias were reactive. The incidence of positivity of the leukemic cells among patients with common B chronic lymphocytic leukemia was surprisingly low (one-third of the patients). The autoantibody nature of the anti-B-cell antibodies and their pathogenic role in the genesis of the patient's hypoimmunoglobulinemia was demonstrated by the effect of removal of antibodies by massive plasmaphereses which were followed by a dramatic and transitory increase of B-cell figures. Whereas most primary immunodeficiency syndromes appear to result from an arrest in the differentiation capabilities of immunologically competent cells, autoantibodies to circulating B lymphocytes may be incriminated in the pathogenesis of some cases of hypogammaglobulinemia.

Adult↗
PubMed1992

[Microscopic colitis and collagenous colitis. An entity not yet reported in Chile].

Collagenous and microscopic colitis have been described as causes for abundant watery diarrhea with a normal radiologic and endoscopic aspect of the colonic mucosa. Microscopic colitis is characterized by diffuse intraepithelial lymphocytic infiltration and collagenous colitis by thickening of subepithelial collagen layer greater than 15 microns with or without inflammatory changes of the mucosa. Here are reported 5 patients with microscopic colitis and 4 with collagenous colitis. The mean age was 52 years (range 40 to 68) with an equal sex distribution. Diarrhea was of longstanding duration without weight loss, anemia or hypoalbuminemia. Occasionally the volume of diarrhea was over 1 L a day. One patient had steatorrhea that proved resistant to a gluten free diet. Endoscopic and radiologic findings were normal in every patient and the diagnosis was based on typical histology. Azulfidine therapy was successful in 7 patients and prednisone in another. Colonic biopsy should be performed in every patient with chronic diarrhea.

Adult↗
PubMed1998

CD45RChighCD4+ intestinal mucosal lymphocytes infiltrating in the inflamed colonic mucosa of a novel rat colitis model induced by TNB immunization.

To clarify the role of CD4(+) intestinal mucosal lymphocytes in chronic intestinal inflammation, we developed a new rat colitis model by immunization with 2,4,6-trinitrobenzenesulfonic acid (TNB) in an emulsion with an adjuvant followed by transrectal administration of a low dose of TNB. Moreover, we assessed the therapeutic effect of anti-CD4 monoclonal antibody (mAb) on this model. In concert with the development ofserum anti-TNB Abs, transmural and segmental colitis that mimics some characteristics of human Crohn's disease was induced in the immunized rats. Immunohistochemical analysis showed the increase of infiltrating lamina propria CD4(+) T cells. Flow-cytometric analysis of isolated cells from inflamed mucosa revealed that CD45RChighCD4(+) T cells were significantly increased. Interestingly, intraperitoneal administration of anti-CD4 mAbs could suppress severe inflammation in the model with decrease of anti-TNB Ab titer. After the treatment with anti-CD4 mAbs, CD45RChighCD4(+) T cells in the lamina propria and interferon-gamma mRNA expression in the colonic lamina propria CD4(+) T cells were decreased. These results indicated that Th1 CD4(+) intestinal mucosal T cells have a role in the progress of inflamed lesions in chronic enteritis. They implicate that a therapy targeting mucosal T cells expressing CD4 may be feasible in the treatment of human Crohn's disease.

Animals↗
PubMed2000

Treatment of experimental colitis by oral tolerance induction: a central role for suppressor lymphocytes.

OBJECTIVE: Inflammatory bowel diseases (IBD) are immune-mediated disorders wherein an imbalance between proinflammatory (Th1) and antiinflammatory (Th2) cytokines is thought to play a role in the pathogenesis. The aim of this study was to test whether induction of oral tolerance to proteins extracted from inflammatory colon alleviates experimental colitis, and whether oral tolerization mediated by suppressor cells can induce immune tolerance. METHODS: Colitis was induced in rats by intracolonic instillation of trinitrobenzenesulfonic acid (TNBS). Rats received five oral doses of colonic proteins extracted from TNBS-colitis colonic wall. Splenocytes harvested from tolerized and control rats were transplanted into irradiated naive rats. RESULTS: Feeding of colitis-extracted proteins ameliorated colonic inflammation, as shown by reduction of colonic ulcerations, as well as decreased diarrhea, intestine and peritoneal adhesions, wall thickness, and edema. A marked reduction of the fraction of injured colonic area and colon weight, and decrease in colon weight, were observed in tolerized rats versus controls. Histological parameters for colitis were markedly improved in tolerized animals that showed significant reduction in inflammatory response and mucosal ulcerations. Tolerized rats developed an increase in TGFbeta1 and a decrease in IFNgamma serum levels. TNBS-induced colitis was significantly attenuated in naive recipients of splenocytes from tolerized rats, compared with rats that received splenocytes from control donors. CONCLUSIONS: Induction of oral tolerance to colitis-extracted proteins downregulates the anticolon immune response, thereby ameliorating experimental colitis. Suppressor lymphocytes mediate the tolerance by induction of a shift from a proinflammatory to an antiinflammatory immune response.

Administration, Oral↗
PubMed1996

Over-utilization of the J delta 3 gene-segment in Crohn's disease.

A majority of normal human intestinal intraepithelial lymphocytes (iIEL) are CD8+, express the alpha beta-T cell receptor (TCR) and are oligoclonal. The remainder of normal iIELs, which are also oligoclonal, express the gamma delta-TCR and preferentially utilize variable regions (V delta 1 and V delta 3) which are different from adult peripheral blood lymphocytes (V delta 2). The junctional region usage of gamma delta-TCRs in intestinal diseases is largely unknown. The aim of this study was to examine gamma delta-T cell clonality and junctional region usage of V delta 1 and V delta 3 transcripts in Crohn's Disease (CD) in comparison to several other chronic inflammatory diseases of the colon by polymerase chain reaction amplification, cloning and sequencing. As previously observed in normal subjects, all inflammatory cases examined, including CD (n = 3), ulcerative colitis (n = 1), diverticulitis (n = 1) and lymphocytic colitis (n = 1), the V delta 1 and V delta 3 transcripts contained reiterated sequences consistent with the expansion of gamma delta-T cells expressing these receptors. In 2/3 CD cases, but none of the non-CD inflammatory cases, transcripts containing J delta 3, a rarely used J delta, was observed among the V delta 1 and/or V delta 3 transcripts. Thus, in a subset of CD, gamma delta-T cells expressing J delta 3 may be expanded implicating a role for unique ligands that drive the expansion of T cells expressing these receptors.

Amino Acid Sequence↗
PubMed2000

Idiopathic enterocolic lymphocytic phlebitis: a rare cause of ischemic colitis.

We report on a 74-year-old female patient who was admitted to the hospital because of abdominal pain. She underwent a colonoscopy and a stenosing mass was found in the cecum. Histologic findings in the biopsy specimens were consistent with ischemic colitis. Due to clinical symptoms and the endoscopic and radiologic findings that roused the suspicion that the patient was suffering from a malignant tumor, a right hemicolectomy was performed. Histology of the resection specimen disclosed an inflammation of the veins. It was characterized by a predominantly lymphocytic infiltration of the vessels affecting the veins of the colonic wall and the mesentery. Furthermore, secondary thrombosis with focal venous occlusion was observed. The colon showed extensive ischemic colitis with focal transmural coagulation necrosis. The disease was considered to be idiopathic lymphocytic phlebitis, which is a rare disease of unknown origin. Our patient is well and alive after more than 1 year, supporting the notion that the disease shows a benign course after surgery.

Aged↗
PubMed1981

Monoclonal B lymphocytes in the peripheral blood of patients with inflammatory bowel disease.

Abnormalities in the B lymphocyte population may be relevant to certain altered in vitro immune responses in patients with inflammatory bowel disease. Using a cytofluorometric detection system, we looked for lymphocytes having homogeneous amounts of surface immunoglobulin of only one light-chain class. We studied the peripheral blood lymphocytes from 20 patients with ulcerative colitis and Crohn's disease. Lymphocytes from 12 of 20 patients (60%) with inflammatory bowel disease expressed abnormal light-chain distributions regardless of disease activity, type of disease, or steroid therapy. None of the 15 age-matched normal controls or 12 patients with other intestinal inflammatory conditions showed abnormal light-chain distributions (p greater than 0.01). The data indicate that there are increased numbers of monoclonal lymphocytes in the peripheral blood of some patients with inflammatory bowel disease. One explanation to account for these findings is the possible presence of an abnormality of immune regulation that permits proliferation of such clones.

Adolescent↗
PubMed2006

Pharmacological effects of ba-wei-xi-lei powder on ulcerative colitis in rats with enema application.

Ba-wei-xi-lei powder is a classical herbal mixture, and is widely used for the treatment of oral ulcer and ulcerative colitis. This study aimed to explore the effect of Ba-wei-xi-lei powder with enema application on ulcerative colitis in rats. Ulcerative colitis was induced by immunization with rabbit's colonic mucosal protein emulsified with Completely Freund's Adjuvant. The mucosal inflammatory reaction and ulcer have been observed in the model rats. Characteristic changes of ulceractive colitis include that CD4 lymphocyte increased in peripheral blood while CD8 lymphocyte decreased; CD8 lymphocyte and TNF-alpha expression area increased in colonic mucosa, while CD4 lymphocyte decreased. Ba-wei-xi-lei powder and sulfasalazine with enema application could alleviate the pathological changes in the model rats. The results suggest that the pharmacological effects of Ba-wei-xi-lei powder on ulcerative colitis in rats are similar to the effect of sulfasalazine.

Animals↗
PubMed2006

Synthesis of 99mTc-HYNIC-interleukin-12, a new specific radiopharmaceutical for imaging T lymphocytes.

PURPOSE: Few radiopharmaceuticals have been described for the study of lymphocyte trafficking despite its high clinical relevance. The main difficulty resides in the identification of a suitable highly specific probe to target these cells. Interleukin-12 (IL12) is a heterodimeric cytokine which plays a key role in the development of Th(1) lymphocytes. The aims of the present study were to label IL12 with (99m)Tc, to evaluate its ability to bind to activated T lymphocytes in vitro and to study its biodistribution in normal mice and mice affected by autoimmune colitis. METHODS: IL12 was derivatised with HYNIC-NHS and labelled with( 99m)Tc. An in vitro binding assay was performed on KIT225 cells, an IL12 receptor-positive cell line. (99m)Tc-IL12 biodistribution in normal mice was studied. Targeting experiments were performed in Balb/c mice injected with KIT225 cells and in mice with chemically induced chronic colitis. RESULTS: (99m)Tc-IL12 labelling efficiency ranged between 75% and 85%. Saturation binding analysis revealed a K (d) of 2.09 nM. Results of biodistribution studies showed a predominant hepatic route of excretion. A significant degree of uptake in the spleen and thymus was also observed. In mice injected with KIT225 cells, (99m)Tc-IL12-specific uptake in these cells increased over time. (99m)Tc-IL12 also accumulated significantly in bowel of mice affected by TNBS-induced colitis showing T lymphocyte infiltration at histology, while accumulation in colon from control animals was negligible. CONCLUSION: We conclude that this radiolabelled cytokine is a suitable candidate for specific in vivo imaging of T lymphocytes: a step forward in molecular imaging of immune-mediated processes.

Animals↗
PubMed2001

Upper gastrointestinal mucosal disease in pediatric Crohn disease and ulcerative colitis: a blinded, controlled study.

BACKGROUND: Upper gastrointestinal endoscopic biopsies often show histologic abnormalities in Crohn disease. Consequently, it has been proposed that routine endoscopy could help to distinguish Crohn disease from ulcerative colitis. Surprisingly, however, recent case reports and an uncontrolled study suggested that similar abnormalities may occur in ulcerative colitis. Therefore, a blinded, controlled study was performed. METHODS: Esophageal, gastric antral, and duodenal biopsies from children with Crohn disease (n = 28) and ulcerative colitis (n = 14) were compared with those from controls undergoing endoscopy for suspected reflux esophagitis (n = 22). Two pathologists, unaware of patient identity and diagnosis, agreed on a consensus report. Severity of inflammation was scored semiquantitatively. Helicobacter pylori colonization was an exclusion criterion. RESULTS: Inflammation was reported as follows: esophagitis: controls 91%; Crohn disease: 72%; ulcerative colitis: 50%; gastritis: controls: 27%; Crohn disease: 92% (P < 0.001); ulcerative colitis: 69%; duodenitis: controls: 9%; Crohn disease: 33%; ulcerative colitis: 23%. In Crohn disease, granulomas were noted in 40% of patients (P = 0.001). Duodenal cryptitis was noted in 26% of patients with Crohn disease but not ulcerative colitis. In one patient with ulcerative colitis, neutrophilic infiltration of gastric glands was seen. Abnormalities seen in Crohn disease and ulcerative colitis included gastroduodenal ulceration (Crohn disease, 7%; ulcerative colitis, 8%), villus atrophy (Crohn disease, 11%; ulcerative colitis, 15%), and increased intraepithelial lymphocytes (Crohn disease, 15%; ulcerative colitis, 31% [P < 0.05]). None of these abnormalities was noted in the controls. CONCLUSION: Although the presence of granulomas can support a diagnosis of Crohn disease, severe inflammation and other abnormalities occur in the proximal gastrointestinal tract in Crohn disease and ulcerative colitis.

Adolescent↗
PubMed2002

Importance of innate immunity and collagen binding integrin alpha1beta1 in TNBS-induced colitis.

Inflammation occurs in the context of integrin-mediated adhesive interactions of cells with their extracellular matrix environment. We investigated the role of the collagen binding integrin alpha1beta1 in a model of colitis. alpha1beta1 was expressed on lamina propria T cells and monocytes during disease. Both alpha1 deficiency and anti-alpha1 mAb treatment (prophylactic and therapeutic) protected against colitis. In vivo alpha1beta1 blockade improved macroscopic and histologic scores, decreased inflammatory cytokine production, and profoundly affected the ability of lamina propria mononuclear cells to proliferate and produce IFN-gamma in vitro. Development and alpha1-mediated inhibition of colitis can be lymphocyte independent, suggesting that activated monocytes also represent a key alpha1beta1-expressing cell type involved in colitis. These results underscore the importance of innate immunity and, specifically, of leukocyte/matrix interactions in regulating local inflammatory responses.

Animals↗
PubMed2004

Higher proliferative capacity of T lymphocytes from patients with Crohn disease than from ulcerative colitis is disclosed by use of Herpesvirus saimiri-transformed T-cell lines.

BACKGROUND: T lymphocytes play a crucial role in the pathogenesis of inflammatory bowel disease. Achieving stable T-cell lines, rather than continuous bleeding of patients, is desirable in order to dissect their implication in the disease. METHODS: Long-lasting T-cell lines from patients with Crohn disease and ulcerative colitis and from healthy volunteers have been obtained by transformation of T lymphocytes using the lymphotropic Herpesvirus saimiri. Lines were subjected to phenotypic and functional analyses, and the results compared with freshly isolated peripheral blood mononuclear cells. RESULTS: Fresh cells revealed only minor differences between patients and controls, with regard to phenotype and proliferative capacity. In contrast, the use of T-cell lines showed that cells from Crohn disease patients, but not ulcerative colitis patients, over-responded to several membrane or cytoplasmic stimuli when compared to control T-cell lines. Thus, higher responses were found when stimulated with alphaCD3 and IL2, alphaCD3 and alphaCD28, IL2 alone, phorbol esters (PMA) and alphaCD3 and, finally, PMA and alphaCD2 (P < 0.05 in all instances). Further, lines from patients with Crohn disease responded more vigorously to alphaCD3 and alphaCD28 or alphaCD3 and PMA when compared to ulcerative colitis (P < 0.05 in both instances). CONCLUSIONS: The data obtained with these lines suggest that T cells from patients with Crohn disease differ in vivo in their proliferative capacity, as compared with those from ulcerative colitis patients, a finding that may reflect the clear Th-1 phenotype found in the former and absent in the latter.

Adult↗
PubMed1982

Anti-colon antibody and lymphocytophilic antibody in ulcerative colitis.

The presence of anti-colon antibody in the sera from patients with ulcerative colitis was demonstrated by antibody-dependent cell-mediated cytotoxicity (ADCC) assay. In addition, the high prevalence of lymphocytophilic antibody in the sera from patients with ulcerative colitis was obtained by fluorescence activated cell sorter (FACS) analysis. This lymphocytophilic antibody was absorbed by rat colon epithelial cells. Moreover the lymphocytes from ulcerative colitis showed lower binding capacity to this antibody, but acquired higher binding capacity after 20 hr incubation at 37 degrees C in vitro. These data suggest that ADCC may have some role in the pathogenesis of ulcerative colitis.

Antibodies↗
PubMed2005

CD4+CD25+ regulatory lymphocytes induce regression of intestinal tumors in ApcMin/+ mice.

Colorectal cancer in humans results from sequential genetic changes in intestinal epithelia commencing with inactivation of the APC tumor suppressor gene. Roles for host immunity in epithelial tumorigenesis are poorly understood. It has been previously shown that CD4+CD25+ lymphocytes inhibit colitis-associated epithelial tumors in Rag-deficient mice. Here we show that addition of CD4+CD25+ lymphocytes in ApcMin/+ mice reduces multiplicity of epithelial adenomas. Interleukin-10 was required in regulatory cells for therapeutic effect. Recipients of regulatory cells showed increased apoptosis and down-regulation of cyclooxygenase-2 within tumors coincident with tumor regression. These data suggest a role for regulatory lymphocytes in epithelial homeostasis in the ApcMin/+ mouse model of intestinal polyposis. Similarities with cancer of the breast, prostate, lung, and other sites raise the possibility of broader roles for regulatory lymphocytes in prevention and treatment of epithelial cancers in humans.

Adenoma↗
PubMed2005

Propionibacterium freudenreichii component 1.4-dihydroxy-2-naphthoic acid (DHNA) attenuates dextran sodium sulphate induced colitis by modulation of bacterial flora and lymphocyte homing.

BACKGROUND AND AIMS: 1.4-Dihydroxy-2-naphthoic acid (DHNA), a bifidogenic growth stimulator from Propionibacterium freudenreichii, is thought to have a beneficial effect as a prebiotic; however, its in vivo effect on intestinal inflammation remains unknown. The aim of this study was to determine whether oral administration of DHNA can ameliorate dextran sodium sulphate (DSS) induced colitis and to determine the possible underlying mechanisms. METHOD: Colitis was induced in mice by treatment with 2.0% DSS for seven days. DHNA (0.6 or 2.0 mg/kg) was given in drinking water prior to (preventive study) or after (therapeutic study) DSS administration. Colonic damage was histologically scored, and mucosal addressin cell adhesion molecule 1 (MAdCAM-1) expression and beta7 positive cell infiltration were determined by immunohistochemistry. mRNA levels of proinflammatory cytokines (interleukin (IL)-1beta, IL-6 and tumour necrosis factor alpha (TNF-alpha)) were determined by quantitative real time polymerase chain reaction. In addition, bacterial flora in the caecum, concentrations of short chain acids, and luminal pH were examined. RESULTS: DHNA improved survival rate and histological damage score in mice administered DSS in both the preventive and therapeutic studies. DHNA significantly attenuated the enhanced expression of MAdCAM-1, the increased beta7 positive cell number, and the increased mRNA levels of IL-1beta, IL-6, and TNF-alpha in DSS treated colon. In addition, the decreased number of Lactobacillus and Enterobacteriaceae induced by DSS was recovered by DHNA. Preventive effects on decrease in butyrate concentration and decrease in pH level in mice administered DSS were also observed in the DHNA preventive study. CONCLUSION: DHNA, a novel type of prebiotic, attenuates colonic inflammation not only by balancing intestinal bacterial flora but also by suppressing lymphocyte infiltration through reduction of MAdCAM-1.

Animals↗
PubMed2004

Imaging of intestinal lymphocyte homing by means of pinhole SPECT in a TNBS colitis mouse model.

BACKGROUND AND AIMS: The increasing knowledge of the molecular basis of leukocyte trafficking results in the development of novel anti-inflammatory strategies for inflammatory bowel disease (IBD). For optimal evaluation of therapy efficacy, information about inflammatory activity in bowel segments or lymphocyte recirculation and kinetics in the follow-up of experimental treatment for IBD is needed. The aim of this study was to evaluate a non-invasive scintigraphic technique, able to assess lymphocyte trafficking in a trinitrobenzene sulfonic acid (TNBS) induced mouse colitis model of IBD. METHODS: TNBS sensitized and non-sensitized murine total splenocytes were labeled in vitro with 111In-oxine and injected into either control or TNBS colitis BALB/c mice. Biodistribution and specific radioactive uptake, representing transferred cells, were determined by serial dedicated animal planar scintigraphy and pinhole SPECT of the abdomen 4, 24 and 48h post injection of labeled cells. In addition, the severity of inflammation was determined by histological scoring. RESULTS: Migration of 111In labeled splenocytes to the colon increased in time and was maximal at 48h after administration. The highest specific radioactive uptake ratio in the colon after 48h was observed in mice with TNBS colitis that received TNBS sensitized lymphocytes. Histological scoring confirmed the presence of colitis in the TNBS treated groups. CONCLUSION: Homing of TNBS-sensitized lymphocytes can be assessed in vivo by means of dedicated animal pinhole SPECT. Generally, this technique enables serial measurement of specific cell trafficking with potential of in vivo evaluation of novel anti-inflammatory strategies in inflammatory bowel disease.

Animals↗