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PubMed1975

[Immunopathology of ulcerative colitis and granulomatous colitis (author's transl)].

There is no convincing evidence as yet for a key role of immunological processes in the pathogenesis of unspecific colitis. However clinical findings as well as immunological data do support the hypothesis that immune reactions are involved primarily or secondarily in the pathogenesis and the clinical course of ulcerative colitis and granulomatous colitis. In such patients a specific adaptation of humoral and cell-bound immune reactions against antigenic material from the colon and other tissues has been found in peripheral blood, lymphatic tissue and bowel wall. In this context it seems to be especially noteworthy, that lymphocytes taken from patients with colitis lead to disintegration of colon epithelial cells in vitro. This cytotoxic effect of the lymphocytes is lost after colectomy or remission of the disease. Ulcerative and granulomatous colitis do have many clinical and immunological peculiarities in common. This makes one think, that possibly the same noxious factors induce differential local reactions because of different hereditary disposition.

Antigen-Antibody Complex↗
PubMed2026

Lymphocyte-C-Reactive Protein Ratio as Promising New Marker for Predicting Surgical Site Infection in Children With Ulcerative Colitis.

BACKGROUND: Surgical site infection (SSI) is a major complication after ileal pouch-anal anastomosis (IPAA) in pediatric ulcerative colitis (UC), significantly impairing quality of life. The lymphocyte-to-C-reactive protein ratio (LCR), a composite marker of systemic inflammation and immune/nutritional status, has emerged as a potential predictor of postoperative outcomes. This study assessed the utility of preoperative LCR in predicting SSI in pediatric UC. METHODS: We retrospectively reviewed pediatric UC patients who underwent IPAA at Mie University Hospital between 2000 and 2024. Preoperative LCR values were analyzed, and the optimal cutoff for SSI prediction was determined using receiver operating characteristic (ROC) analysis. Multivariate logistic regression was performed to identify independent risk factors. SSI was defined according to CDC criteria within 30&#x2009;days postoperatively. RESULTS: Among 57 patients, 11 (19.3%) developed SSI. The incidence was higher in three-stage procedures than in two-stage procedures (22.7% vs. 17.1%). In both groups, preoperative LCR was significantly lower in SSI-positive patients. ROC analysis demonstrated good discrimination (AUC: 0.80), with an optimal cutoff of LCR <&#x2009;5000 (sensitivity: 90.9%, specificity: 71.7%). Multivariate analysis confirmed LCR <&#x2009;5000 as an independent predictor of SSI (odds ratio [OR]: 6.34, 95% CI: 1.23-48.2, p&#x2009;=&#x2009;0.027). CONCLUSION: Preoperative LCR is a simple, objective biomarker that reliably predicts SSI risk in pediatric UC patients undergoing IPAA. Incorporating LCR into preoperative risk stratification may enable personalized interventions, including nutritional optimization and tailored prophylaxis, to improve surgical outcomes.

inflammatory bowel disease↗
PubMed1998

Cytokine production from colonic T cells in patients with ulcerative colitis with and without primary sclerosing cholangitis.

PURPOSE: Only five percent of all patients with ulcerative colitis develop primary sclerosing cholangitis. T cells accumulate at the sites of the colonic and bile duct inflammation in both ulcerative colitis and primary sclerosing cholangitis. T helper cell populations comprise functionally distinct subsets characterized by the cytokines they produce. Several alterations in cytokine production have been described in patients with ulcerative colitis. The aim of this study was to investigate possible differences in T helper subsets and cytokine production in peripheral blood and colonic mucosa among ulcerative colitis patients with and without primary sclerosing cholangitis. METHODS: Eleven patients with primary sclerosing cholangitis and extensive ulcerative colitis, 11 patients with extensive ulcerative colitis and no liver disease, and 5 patients without any history of liver disease who underwent routine colonoscopy because of previous polypectomy were included in the study. Colonoscopy with multiple biopsies was performed on all patients. Lamina propria mononuclear cells and peripheral blood mononuclear cells were isolated. A modified version of solid-phase enzyme-linked immunospot assay was used for the separate counting of cells producing interferon-gamma, interleukin-2 (T helper 1), and interleukin-4 (T helper 2). RESULTS: No differences in spontaneous production of cytokines from peripheral blood mononuclear cells was found among the three groups. Patients with primary sclerosing cholangitis compared with patients with ulcerative colitis without liver disease showed a significant increase in the number of cells secreting interferon-gamma after purified protein derivative stimulation (P < 0.02). More cells secreting interferon-gamma were found in the two ulcerative colitis groups than in the cell populations from healthy controls (P < 0.03). The number of cells secreting interferon-gamma in the primary sclerosing cholangitis group was significantly lower than in the ulcerative colitis group without liver disease (P < 0.04). The number of cells secreting interleukin-4 was lower in the primary sclerosing cholangitis group than among the patients with ulcerative colitis only (P = 0.05). CONCLUSION: Isolated lymphocytes from colonic mucosa differ in cytokine production in patients with ulcerative colitis with and without primary sclerosing cholangitis.

Cholangitis, Sclerosing↗
PubMed1997

Non-infective colitis in infancy: evidence in favour of minor immunodeficiency in its pathogenesis.

Forty two infants below the age of 2 years presenting with chronic non-infective diarrhoea and shown to have histologically proved colitis were investigated over a five year period. Allergic colitis was the most common cause of colitis, accounting for 62% of the cases. Other colitides diagnosed included: non-specific colitis, autoimmune enterocolitis, and ulcerative colitis accounting for 10% each; severe combined immunodeficiency 7%, and Crohn's disease 3%. A positive family history and a personal history of atopy were obtained in 48% and 29% of the cases respectively. Serum immunoglobulin A, IgG2, and IgG4 were very low in over 50% of the entire cohort of infants with colitis; 66% of those with severe combined immunodeficiency, autoimmune enterocolitis, and ulcerative colitis (n = 11) had low CD3 and CD4 T lymphocytes with an accompanying increase in CD8 in two thirds of those with severe combined immunodeficiency. T lymphocytes were normal in those with allergic colitis. Thus infants with proved non-infective colitis as a group show a high prevalence of IgA, IgG2, and IgG4 deficiency. It is likely that this minor deficiency of mucosa associated immunoglobulin production has a role in the pathogenesis of the colitic process.

Autoimmune Diseases↗
PubMed2000

Mice with a selective deletion of the CC chemokine receptors 5 or 2 are protected from dextran sodium sulfate-mediated colitis: lack of CC chemokine receptor 5 expression results in a NK1.1+ lymphocyte-associated Th2-type immune response in the intestine.

The chemokine receptors CCR2 and CCR5 and their respective ligands regulate leukocyte chemotaxis and activation. To determine the role of these chemokine receptors in the regulation of the intestinal immune response, we induced colitis in CCR2- and CCR5-deficient mice by continuous oral administration of dextran sodium sulfate (DSS). Both CCR2- and CCR5-deficient mice were susceptible to DSS-induced intestinal inflammation. The lack of CCR2 or CCR5 did not reduce the DSS-induced migration of macrophages into the colonic lamina propria. However, both CCR5-deficient mice and, to a lesser degree, CCR2-deficient mice were protected from DSS-induced intestinal adhesions and mucosal ulcerations. CCR5-deficient mice were characterized by a greater relative infiltration of CD4+ and NK1.1+ lymphocyte in the colonic lamina propria when compared to wild-type and CCR2-deficient mice. In CCR5-deficient mice, mucosal mRNA expression of IL-4, IL-5, and IL-10 was increased, whereas that of IFN-gamma was decreased, corresponding to a Th2 pattern of T cell activation. In CCR2-deficient mice, the infiltration of Th2-type T cells in the lamina propria was absent, but increased levels of IL-10 and decreased levels of IFN-gamma may have down regulated mucosal inflammation. Our data indicate that CCR5 may be critical for the promotion of intestinal Th1-type immune responses in mice.

Animals↗
PubMed1994

Studies on the enteropathy associated with primary hypogammaglobulinaemia.

Twelve patients with primary hypogammaglobulinaemia with diarrhoea not associated with known microbial pathogens were investigated. Histological evidence of inflammation was common in the stomach and jejunum. Moreover, eight of 10 patients undergoing colonoscopy had low grade 'microscopic colitis' with raised intraepithelial lymphocytes and an intact crypt architecture. Five of 12 patients had small intestinal inflammation on 111indium leucocyte scintigrams and all had increased faecal excretion (normal < 1%) of 111indium (over four days), which varied in intensity from mild (faecal excretion of 111indium = 1-3%) to that comparable with moderately active (7-14.5%) Crohn's disease. Three patients had small intestinal strictures superficially resembling Crohn's disease. Histologically, however, these lacked characteristic diagnostic features of Crohn's disease in two and the third patient had non-steroidal anti-inflammatory drug induced diaphragm like strictures. Six of seven who were most severely symptomatic were successfully treated with an elemental diet with rapid improvement of symptoms. The faecal excretion of 111indium was repeated in five and all improved but histologically the colitis remained unchanged. These studies show that some patients with primary hypogammaglobulinaemia have intestinal inflammation unlike that found in classic inflammatory bowel disease. Elemental diet is a useful temporary measure in the treatment of these patients.

Agammaglobulinemia↗
PubMed1991

Coexpression of CD4 and CD8 on peripheral blood T cells and lamina propria T cells in inflammatory bowel disease by two colour immunofluorescence and flow cytometric analysis.

Using two colour immunofluorescence with fluorescein isothiocyanate and phycoerythrin labelled monoclonal antibodies and multiparameter flow cytometry, we investigated the coexpression of CD4 and CD8 antigens on peripheral blood lymphocytes and lamina propria lymphocytes of patients with ulcerative colitis and Crohn's disease and normal control subjects. Both the absolute number and the proportion of peripheral blood CD4+, CD8+ cells in inflammatory bowel disease were small but significantly increased compared with those in normal control subjects. Peripheral blood lymphocytes activated with phytohaemagglutinin showed appreciably increased coexpression of CD4+, CD8+. These CD4, CD8 positive cells were large and granular. Thus the increased number of peripheral blood CD4+, CD8+ cells in inflammatory bowel disease suggests that chronic immune activation occurs not only in the active state of the disease but also in remission. The proportion of CD4+, CD8+ cells in the lamina propria was greater than in peripheral blood in normal subjects, suggesting chronic immune stimulation of the local immune system. This was also seen in patients with Crohn's disease or inactive ulcerative colitis. The proportion of CD4+, CD8+ cells was, however, significantly less in the lamina propria of patients with active ulcerative colitis. Whether this implies a possible defect in mucosal immunoregulation in active ulcerative colitis cannot be determined from these results.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1999

The role of CD4+ lymphocytes in the susceptibility of mice to stress-induced reactivation of experimental colitis.

Idiopathic inflammatory bowel disease is a chronic relapsing condition. The role of stress in causing relapses of inflammatory bowel disease remains controversial. We now show that colitis induced in mice by dinitrobenzenesulfonic acid (DNBS) resolves by 6 weeks, but can subsequently be reactivated by stress plus a sub-threshold dose of DNBS, but not by DNBS alone. Stress reduced colonic mucin and increased colon permeability. Susceptibility to reactivation by stress required CD4+ lymphocytes and could be adoptively transferred. We conclude that stress reactivates experimental colitis by facilitating entry of luminal contents that activate previously sensitized CD4 cells in the colon.

Adoptive Transfer↗
PubMed1988

Interleukin 2 receptor expression by macrophages in inflammatory bowel disease.

The expression of interleukin 2 receptor by macrophages from normal and inflamed terminal ileum and colon has been studied by using two monoclonal antibodies. In tissue sections from normal ileum and colon, scattered positive lymphocytes and only occasional weakly positive macrophages were seen. In ileal and colonic Crohn's disease or ulcerative colitis many positive macrophages and lymphocytes were seen in the lamina propria. These findings were confirmed by staining cytospin preparations of isolated intestinal mononuclear cells. The isolated macrophages were able to phagocytose opsonized zymosan and the majority were able to undergo a respiratory burst when triggered with opsonized zymosan or phorbol myristate acetate (PMA), suggesting that they were activated. Stimulation with interferon-gamma or lipopolysaccharide did not increase the number of macrophages staining with the antibodies to the interleukin 2 receptor. Therefore we postulate that a large majority of the macrophages expressing interleukin 2 receptor in inflammatory bowel disease are a recently recruited population of cells.

Antibodies↗
PubMed1996

Tolerability and activity of a new recombinant interferon-alpha B/D hybrid in patients with HIV-1 infection.

The maximum tolerated dose (MTD) and toxicity profile of a new recombinant interferon-alpha B/D hybrid (IFN-alpha B/D) in HlV-1-infected patients were determined in an outpatient, dose-escalating study with dose groups of three patients: 16, 32, 48, 64, 96 and 112 million international units (MIU) three times weekly subcutaneously during 12 weeks. The MTD was the last dose level just below the dose level at which more than one patient experienced > or = grade 3 toxicity. The study also searched for preliminary evidence of efficacy of IFN-alpha B/D. Sixteen HIV-1-infected patients with CD4 cell counts > or = 200/mm3 were enrolled: eight were asymptomatic and eight had symptomatic disease. Two patients were excluded as a result of protocol violations. Five patients (36 per cent; one at each tested dose level) discontinued prematurely due to side effects. One patient was lost to follow-up. Twelve patients (87 per cent) experienced > or = grade 2 toxicity. Toxicity > or = grade 3 occurred in none of three patients assigned to 16 MIU, one of five assigned to 32 MIU (fatigue), one of three assigned to 48 MIU (haemorrhagic colitis) and two of three assigned to 64 MIU (fatigue). One patient (48 MIU) had reversible cardiomegaly. Progressive weight loss was experienced by 12 of 14 participants. Serum HIV-1 p24 antigen declined in nine of 11 antigenaemic patients (seven persistently > 50 per cent) without a clear dose-response relationship. CD4 percentages showed no consistent pattern and T cell reactivity diminished. The tolerability and toxicity profile of IFN-alpha B/D appear to be fairly similar to that of other types of IFN-alpha.

Administration, Cutaneous↗
PubMed2026

An inflammatory bowel disease-linked lncRNA suppresses transcription factor T-BET expression in T cells to limit intestinal inflammation.

Among the tens of thousands of annotated long noncoding RNAs (lncRNAs) in the human genome, only a small fraction have been functionally characterized. Here, we show that a well-established inflammatory bowel disease (IBD) risk locus encoded a conserved lncRNA, lnc15 (2310015A10Rik/ENSMUSG00000097729), whose structure was destabilized by risk-associated variants, leading to its degradation. Deletion of lnc15 in mice resulted in molecular features of inflammation under steady-state conditions and conferred heightened susceptibility to experimental colitis. Lnc15 was abundantly expressed in T cells, with highest expression in regulatory T (Treg) cells. Mechanistically, lnc15 suppressed the transcription factor T-BET by recruiting the CCR4-NOT RNA degradation complex to Tbx21 mRNA. Our study identifies that lnc15 simultaneously enhances Treg cell suppressive function and impairs conventional T cell pathogenicity in the context of intestinal inflammation. Collectively, these findings identify lnc15 as a functional lncRNA that links noncoding genetic variation to immune regulation and prevention of mucosal inflammation. VIDEO ABSTRACT.

RNA, Long Noncoding↗
PubMed1997

Non infective colitis in infancy: evidence in favour of minor immunodeficiency in its pathogenesis.

Forty two infants below the age of two years presenting with chronic non infective diarrhoea and shown to have histologically proven colitis were investigated over a five year period at this hospital. Allergic colitis was the most common cause of colitis accounting for sixty two percent of the cases. Other colitides diagnosed included: non specific colitis, autoimmune enterocolitis and ulcerative colitis accounting for 9.5% each, severe combined immunodeficiency 7.1% and Crohn's disease 2.8%. A positive family history and a personal history of atopy was obtained in 47.6% and 28.6% of the cases. Serum immunoglobulin A, IgG2 and IgG4 were very low in over 50% of the infants with colitis. Sixty six percent of those with severe combined immunodeficiency, autoimmune enterocolitis and ulcerative colitis (n = 11) had low CD3 and CD4 T lymphocytes with an accompanying elevated CD8 in 2/3 of those with severe combined immunodeficiency. T lymphocytes were normal in those with allergic colitis. We conclude that infants with proven non infective colitis show as a group a high prevalence of IgA, IgG2 and IgG4 deficiency. It is likely that this minor deficiency of mucosal associated immunoglobulin production have a role in the pathogenesis of the colitic process.

Autoimmune Diseases↗
PubMed1996

Human immunodeficiency virus infection, the acquired immunodeficiency syndrome, and inflammatory bowel disease.

The objective of this study was to determine the effect of human immunodeficiency virus (HIV) infection/acquired immunodeficiency syndrome (AIDS) on inflammatory bowel disease (IBD). A retrospective survey of the medical records of St. Paul's Hospital and its AIDS-care physicians/gastroenterologists searching for patients with both HIV/AIDS and IBD was conducted. Of 1,839 hospitalized patients (4,459 hospital admissions) from 1989 to 1993, two patients with AIDS/HIV and IBD were found. The physician survey revealed four patients for a total of six patients. Four patients developed de novo IBD--two ulcerative colitis (UC), one Crohn's disease (CrD), and one indeterminate colitis (IC)--after HIV infection. Two patients had UC predating HIV seroconversion. The absolute CD4 count of patients with de novo IBD was 210-700 cells/ml at the time of IBD. The patient with IC maintained quiescent IBD from a CD4 count of 190-30 cells/ml. The other had many relapses before HIV seropositivity. With CD4 count depletion, disease activity improved. IBD medications were discontinued at a CD4 count of 130 cells/ml. Diarrhea returned at a CD4 count of 20 cells/ml; however, sigmoidoscopy was unremarkable, and mucosal biopsy revealed cryptosporidiosis without active UC. No patient had an AIDS-related illness during active IBD. Two patients followed to CD4 counts of < 30 cells/ml suffered AIDS-related infections with quiescent IBD. With a progressive decline in CD4 count, IBD disease activity may improve and remit. The CD4 count at which remission occurs may reflect severe immunodeficiency such that risk for AIDS-related infection is high. Active IBD may occur with lesser degrees of immunodeficiency.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Specificity of antibodies secreted by hybridomas generated from activated B cells in the mesenteric lymph nodes of patients with inflammatory bowel disease.

Hybridomas have been prepared from active B cells in lymphoid tissue draining lesions of Crohn's disease (CD) and ulcerative colitis (UC), by fusion of fresh mesenteric lymph node suspensions with the murine JK myeloma. Two hundred and fifty nine immunoglobulin secreting hybridomas have been obtained from nine patients. The antibodies have been screened for binding to food antigens, sections of human gut, and bacteria including two unidentified acid fast isolates from CD lymph nodes. Autoantibodies, and antibodies to food antigens implicated by others in the aetiology of CD were rare, comprising 1.2%, and 2.5% respectively. Most donors yielded none of these. Thus neither food antigens nor autoantigens are major antigenic stimuli in nodes draining inflammatory bowel disease. On the other hand between 19% and 83% of supernatants from different donors bound to one or more bacterial genus. The mycobacteria and the CD isolates were amongst the genera to which most antibodies bound, though binding to E coli was more frequent. Significantly more CD than UC derived supernatants bound to BCG. As mycobacteria are not though to be part of the normal bowel flora, the high percentage of hybridomas secreting antibodies which bind to this genus is surprising.

Adult↗
PubMed2006

DX5+ NKT cells induce the death of colitis-associated cells: involvement of programmed death ligand-1.

NKT cells are activated by CD1d and show an immune regulating function. Here, we investigated whether DX5+ NKT cells could be used to reduce colitis in a chronic colitis mouse model and studied the potential immunological mechanisms involved. Chronic colitis was induced either by transfer of enriched CD62L+ CD4+ T cells to severe-combined-immunodeficient mice or by feeding dextran sodium sulfate to immune competent mice. DX5+ NKT cells were transferred to mice with chronic colitis. Co-transfer of DX5+ NKT cells, but not CD8+ control cells, prevented the onset of colitis, and the immune regulatory effect of DX5+ NKT cells was completely abrogated by injecting CD1d blocking antibody. Moreover, DX5+ NKT cells reduced established colitis in both chronic colitis models. In vitro, DX5+ NKT cells induced cell death of colon-infiltrating lymphocytes isolated from diseased mice. This effect was inhibited in the presence of either anti-CD1d or anti-programmed death ligand-1 (PD-L1) blocking antibodies. The specific potency of DX5+ NKT cells in regulating chronic colitis in two mouse models is demonstrated. In vitro testing suggests that DX5+ NKT cells activated by CD1d induce cell death of colitis-inducing lymphocytes, which is mediated through PD-L1. Therefore, DX5+ NKT cells could be important in the regulation of immune responses associated with chronic colitis.

Adoptive Transfer↗
PubMed2005

Effects of garlicin on apoptosis in rat model of colitis.

AIM: To investigate the effects of garlicin on apoptosis and expression of bcl-2 and bax in lymphocytes in rat model of ulcerative colitis (UC). METHODS: Healthy adult Sprague-Dawley rats of both sexes, weighing 180+/-30 g, were employed in the present study. The rat model of UC was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) enema. The experimental animals were randomly divided into garlicin treatment group (including high and low concentration), model control group, and normal control group. Rats in garlicin treatment group and model control group received intracolic garlicin daily at doses of 10.0 and 30.0 mg/kg and equal amount of saline respectively 24 h after colitis model was induced by alcohol and TNBS co-enema. Rats in normal control group received neither alcohol nor only TNBS but only saline enema in this study. On the 28th d of the experiment, rats were executed, the expression of bcl-2 and bax protein was determined immunohistochemically and the apoptotic cells were detected by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate fluorescence nick end labeling (TUNEL) method. At the same time, the rat colon mucosal damage index (CMDI) was calculated. RESULTS: In garlicin treatment group, the positive expression of bcl-2 in lymphocytes decreased and the number of apoptotic cells was more than that in model control group, CMDI was lower than that in model control group. The positive expression of bax in lymphocytes had no significant difference. CONCLUSION: Garlicin can protect colonic mucosa against damage in rat model of UC induced by TNBS enema.

Allyl Compounds↗
PubMed2003

Effects of Rheum tanguticum polysaccharide on TNBS -induced colitis and CD4+T cells in rats.

AIM: To study the effects of Rheum tanguticum polysaccharide(-1) (RTP(-1)) on ulcerative colitis in rats induced by 2, 4, 6-trinitrophene sulphonic acid (TNBS) and their possible mechanism. METHODS: RTP1 (200 mg.kg(-1), i.g.) extracted from Rheum tanguticum Maxim. ex Regel was administrated to rats with colitis induced by TNBS for 5 d, 7 d, 10 d and 14 d, respectively. The effects of RTP1 and dexamethasone (DX, 0.2 mg.kg(-1), i.g.) were contrastively investigated. The MPO level and SOD activity were determined by chromatometry. The expansion and protein expression of CD4+T lymphocytes isolated from colon mucosae and mesenteric lymph nodes of colitis rats were performed by immunohistochemical analysis and Western-blot methods. RESULTS: Treatments of RTP1 (200 mg.kg(-1), i.g.) significantly reduced diarrhea, mortality, colon mass, ulcer areas and MPO level in colon mucosae on days 5, 7, 10 and 14 (5.2+/-1.4, 5.4+/-0.7, 5.2+/-1.8, P<0.05. 3.4+/-0.8, P<0.01. 16.1+/-12.1, P<0.01. 31.8+/-8.6, 17.7+/-5.3, 12.7+/-4.1, P<0.05). The effects of RTP1 were similar to those noted above in DX group, but there were no immunosuppressive effects of DX in RTP(-1) group, such as body mass loss, thymus and spleen atrophy. The decreased number and down-regulated protein levels of CD4+T cells isolated from the colon of colitis rats treated with RTP1 were found. CONCLUSION: RTP1 shows significantly protective effects but lower side effects on rats with colitis induced by TNBS. The mechanism may be due to the resistance to over expansion of CD4.

Animals↗