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PubMed2006

Antisense therapy of MAdCAM-1 for trinitrobenzenesulfonic acid-induced murine colitis.

BACKGROUND: Anti-alpha4 integrin reagent, natalizumab, which is 1 of the most promising antiadhesion monoclonal antibodies, has been introduced into clinical trials against inflammatory bowel disease (IBD). Lethal consequences such as progressive multifocal leukoencephalopathy have recently been reported in patients using natalizumab, making it critical to determine which selective adhesion molecule in the alpha4 integrins-dependent pathway should be targeted for inhibition and the minimal spectrum of activity required for the valid treatment of IBD. Mucosal addressin cell adhesion molecule (MAdCAM)-1 is known to be restrictedly expressed in gut-associated lymphoid tissues, and its expression dramatically increases in IBD. This study aimed to reevaluate the effectiveness of MAdCAM-1 inhibition and to determine the feasibility of anti-MAdCAM-1 strategy. MATERIALS AND METHODS: Antisense MAdCAM-1 oligonucleotides were injected into mice at 1.5 mg/kg/day for 7 consecutive days from the first day of a trinitrobenzene sulfonate enema. RESULTS: MAdCAM-1 antisense oligonucleotides significantly suppressed the development of trinitrobenzene sulfonate colitis clinically and histopathologically compared with controls. Immunohistochemistry and semiquantitative reverse-transcription polymerase chain reaction of the colon tissues revealed that MAdCAM-1 protein and mRNA expression were lower in antisense-treated mice than in controls. In addition, MAdCAM-1 antisense treatment reduced the number of alpha4beta7 lymphocytes in the inflamed colonic mucosa. CONCLUSIONS: These data suggest that antisense suppression of MAdCAM-1 is of equivalent effectiveness to that of anti-MAdCAM-1 or anti-alpha4 integrin antibody in previous reports and could be a new therapy for IBD.

Animals↗
PubMed1998

Expression of inducible nitric oxide synthase activity in human colon epithelial cells: modulation by T lymphocyte derived cytokines.

BACKGROUND: Nitric oxide (NO) synthesis and inducible nitric oxide synthase (iNOS) expression are increased in colonic biopsy specimens from patients with ulcerative colitis, but the cellular source of NO production is not known. AIMS: To examine the distribution of iNOS in human colonic mucosa and to explore the ability of T lymphocyte derived cytokines to regulate iNOS expression and activity in human colonic epithelial cells. METHODS: iNOS expression was examined using immunohistochemistry in colonic biopsy samples from 12 patients with ulcerative colitis and three with infectious colitis and compared with 10 normal controls. In vitro iNOS expression and activity were determined in HT-29 cell cultures; nitrite levels were measured using a fluorescent substrate, iNOS mRNA expression by northern blot analysis, and iNOS protein expression by western blot analysis. RESULTS: No iNOS expression was detected (10 of 10) in non-inflamed mucosa derived from normal controls. In 11 of 12 cases of newly diagnosed ulcerative colitis, iNOS protein was expressed in the epithelial cells, while no other positive cells were found in the lamina propria. Similar iNOS labelling was found in colonic biopsy samples from patients with infectious colitis in the acute phase, but when re-examined in samples from patients in total remission, no iNOS staining was observed. Both interleukin (IL)-13 and IL-4, but not IL-10, are potent inhibitors of iNOS expression and activity induced by an optimal combination of cytokines, namely IL-1 alpha, tumour necrosis factor alpha and interferon gamma. CONCLUSIONS: The data suggest that the epithelium is the major source of iNOS activity in ulcerative colitis and that IL-13 and IL-4 may act as intrinsic regulators of NO generation in intestinal inflammation.

Acute Disease↗
PubMed1989

[Molecular genetic detection of polyclonal immune response in autoimmune thyroiditis and inflammatory bowel diseases].

Southern blot hybridization techniques were used to analyze the arrangements of the immunoglobulin and the T cell antigen receptor genes in lymphocytes of patients with Graves disease and Hashimoto's thyroiditis as well as in patients with Crohn's disease, chronic ulcerative colitis, and with other gastrointestinal disease. The results indicate that the immune response of autoimmune thyroid disease and inflammatory bowel disease is of polyclonal origin.

Adolescent↗
PubMed1996

Selective immunomodulation in patients with inflammatory bowel disease--future therapy or reality?

Knowledge of the aetiology and pathogenesis of the inflammation in ulcerative colitis and Crohn's disease is still insufficient. It is thought that some antigen is the trigger which induces a chain of immune reactions but the origin of this antigen has not so far been elucidated. In theory, an antigen-presenting cell forms a complex with endotoxin-derived peptides as antigen. T-helper lymphocytes recognize this complex, are activated and start to produce cytokines. For inflammatory bowel diseases (IBD) the most important cytokines identified are interleukin 1 (IL-1), interleukin 2 (IL-2), interleukin 6 (IL-6), interleukin 8 (IL-8), gamma-interferon (G-IFN), and tumor necrosis factor-alpha (TNF-alpha). Inhibition of these cytokines can be achieved by administration of cyclosporine, which inhibits the function of T-helper lymphocytes. Orally, intravenously, and locally administered cyclosporine is able to improve the disease activity in ulcerative colitis and Crohn's disease, but its use is limited because of side-effects. The novel immunosuppressant FK506 has comparable actions to cyclosporine in regulating cytokine production and may even be more effective than cyclosporine. The receptor antagonist of IL-1 (IL-1ra) competitively binds to the IL-1 receptor located on several lymphocytes. Treatment of animals with IL-1ra has been successful and clinical trials using recombinant IL-1ra are underway in IBD. Antibodies against alphaIL-2r have also been used successfully in animal studies. No experience with this substance has been obtained in man. The use of alpha-interferon seems to be effective in some patients with Crohn's disease. CD4 and CD8 molecules on lymphocytes are needed to form the interaction between antigen, antigen-presenting cell, and lymphocytes. Specific monoclonal antibodies against CD4 are successfully used in patients with active ulcerative colitis and Crohn's disease. TNF-alpha shares many of the proinflammatory activities of IL-1. In preliminary studies, especially in patients with Crohn's disease, the effects of the administration of antibodies to TNA-alpha were excellent.

Colitis, Ulcerative↗
PubMed1987

Molecules controlling lymphocyte-endothelial interactions in lymph nodes are produced in vessels of inflamed synovium.

In vitro lymphocyte adhesion to, and selective radiosulphate uptake by, endothelial cells has been demonstrated in diseased synovium of patients with rheumatoid disease, osteoarthritis, and the peripheral arthropathy associated with ankylosing spondylitis and ulcerative colitis. These characteristics have been described previously in endothelial cells functionally specialised for promoting lymphocyte traffic from blood to lymph node parenchyma. It is suggested that these observations indicate that some synovial vessels may be responsible, at least in part, for the selective accumulation of lymphocytes in the tissue. Manipulation of the development of this type of vessel may offer a novel way of influencing the progress of inflammatory arthropathies.

Arthritis, Rheumatoid↗
PubMed2003

CCR4 is an up-regulated chemokine receptor of peripheral blood memory CD4+ T cells in Crohn's disease.

Several chemokine receptors are expressed selectively on the surface of T cells depending on their polarization. The aim of this study was to characterize chemokine receptor expression in peripheral blood memory T cells in Crohn's disease (CD) and ulcerative colitis (UC), and to correlate the expression with disease activity. Peripheral blood mononuclear cells (PBMCs) were obtained from 24 patients with CD, 30 patients with UC, 24 normal controls and 10 disease controls. PBMCs were stained by anti-CCR3, CCR4, CCR5, CXCR3, CD4, CD8, CD45RO and beta 7 integrin, and the expression of the chemokine receptors were determined by flow cytometry. CCR4 expression on memory T cells was significantly lower in UC than in CD or normal controls, and that of memory CD4+ T and beta 7(high) memory CD4+ T cells was significantly higher in CD than in UC or normal controls. CCR4 expression on memory CD4+ T cells exhibited significant positive correlation with disease activity in CD, and this decreased significantly after treatment. Such a decrease was not found in the disease controls. CCR5 and CXCR3 expression on memory CD8+ T cells was significantly lower in CD than in normal controls. CXCR3 expression on beta 7(high) memory CD4+ T and CXCR3 expression on memory CD8+ T cells were lower in UC than in normal controls. These findings suggest that in peripheral blood memory T cells, chemokine receptor expression is different between CD and UC. Enhancement of CCR4 and suppression of CCR5 and CXCR3 seem to be the characteristic chemokine receptor profile in peripheral blood memory T cells of CD.

Acute Disease↗
PubMed1994

[Clinical study in treating intractable ulcerative colitis with traditional Chinese medicine].

UNLABELLED: Clinical double blind study in treating 153 intractable ulcerative colitis with Chinese medicinal herbs was conducted, the patients were randomly assigned to three groups. Group I is administered with Jian Pi Ling (JPL) tablet with retention-enema of Radix Sophorae Flavescentis and Flos Sophora (RSF-FS) decoction per night, group II with salicylazosulfapyridine (SASP) and retention-enema of dexamethasone, group III with placebo and retention-enema of decoction as that in group I. After 90 days every patients were checked by means of fibro-enteroscope, pathologic and immunologic parameters. THE RESULTS: the curative rates of group I, II, III, were 53.1%, 27.7% and 19.0%, the total effective rates were 85.9%, 59.6% and 45.2% respectively. By comparison among groups, the efficacy of group I was the best (P < 0.01). The check of T and B lymphocyte subpopulation showed the B lymphocyte of group I markedly decreased, OKT3 and OKT8 obviously increased, the ratio of OKT4 and OKT8 approached normal value. The amount of IgG, IgM, C3 increased abnormally, decreased dramatically after medication, while those of group II and III have not changed significantly. The bacteriostatic test in vitro showed the bacteriostatic effect of RSF-FS on pathogenic B. coli, Shigella dysenteriae and Staphylococcus aureus was the best, that of solution Jian Pi Ling the next, that of SASP was the least effective. Therefore, the principle and method of group I seems to be the best therapeutic programme.

Administration, Rectal↗
PubMed1987

A case of salicylazosulfapyridine (Salazopyrin)-induced acute pancreatitis with positive lymphocyte stimulation test (LST).

A case of acute pancreatitis induced by salicylazosulfapyridine (Salazopyrin, SASP) was reported. A 33-year-old man with ulcerative colitis was given SASP. Five weeks later, P-type serum amylase was found to be elevated. The amylase/creatinine clearance ratio (ACCR) and serum lipase were also elevated. There were neither subjective symptoms nor abnormal ultrasound findings in the pancrease. Lymphocyte stimulation test (LST) to SASP was positive. Asymptomatic pancreatitis by SASP was suspected and SASP administration was halted. Afterwards the abnormal data became normal. Readministration of SASP because of relapse caused an episode of pancreatitis similar to the first occasion. LST was negative before SASP intake and became positive after intake. Desensitization to SASP was unsuccessful. LST was negative before attempting desensitization and became positive when the dosage of SASP increased to 100 mg daily. This is the second case of acute pancreatitis reported to be induced by SASP and this is the first case in which LST to SASP was described. To our knowledge, this is also the first case in which a positive LST was described in drug-induced pancreatitis. This case provides evidence for the role of delayed type hypersensitivity in the etiopathogenesis of SASP allergy and of dose-independent drug-induced pancreatitis.

Acute Disease↗
PubMed1996

Similarities and dissimilarities between asthma and inflammatory bowel diseases.

Because both asthma and inflammatory bowel disease are chronic relapsing inflammatory conditions, comparisons are inevitable. Both disorders reflect the convergence of environmental trigger factors in genetically predisposed individuals. The genetic preposition may be on a polygenic basis or on the basis of genetic heterogeneity. Environmental factors that may trigger the expression or relapse in asthma and inflammatory bowel disease include: cigarette smoking (in Crohn's but not in ulcerative colitis), the use of non-steroidal anti-inflammatory drugs in asthma and Crohn's disease), infection and possibly stress. TH lymphocytes are currently believed to be important in asthma and in Crohn's disease but not in ulcerative colitis. IgE-activated eosinophils and mast cells are central to the maintenance of asthma but do not play such a crucial role in inflammatory bowel disease. TH2 cytokines including IL-4 and IL-5 are believed to be important in the inflammatory response of asthma, and TH cytokines are believed to be in Crohn's disease but a TH1 or TH2 subclassification is not currently evident. The hallmark of asthma is increased reactivity of the airways, in terms of bronchoconstriction. Altered physiology also accompanies inflammatory bowel disease but hyperactivity is not an invariable feature. Finally, it is becoming increasingly evident that neural influences modulate inflammatory processes and this is likely to be relevant to both asthma and inflammatory bowel disease.

Animals↗
PubMed2004

Partial protection against dextran sodium sulphate induced colitis in histamine-deficient, histidine decarboxylase knockout mice.

OBJECTIVES: Chemically induced mucosal inflammation in animal models is a suitable tool for studying factors in the pathogenesis of inflammatory bowel disease. The aim of this study was to determine whether absence of histamine has an effect on the development of experimental colitis. METHODS: Histamine-deficient, histidine decarboxylase (HDC) knockout Balb/c mice and genetically identical control animals with intact HDC were studied. Colitis was induced by the administration of 2% dextran sodium sulphate in drinking water. Mice were killed after 5 days and disease activity assessed by clinical, histologic, and immunohistologic parameters. Bacterial components of stool were examined. RESULTS: Clinical disease activity was higher in the mice with intact HDC (disease activity index, 2.21) than in the histamine-deficient knock-out mice (1.88). Histologic findings were similar in the two groups. On day 5, the inflammation score of the HDC sufficient group was 5.25 (+/-1.055) and the crypt score was 5.00 (+/-1.128). The scores in the HDC knock-out group were 4.667 (+/- 0.707) and 4.667 (+/- 0.86), respectively. There was a significant difference in the number of interleukin (IL-10)-producing lymphocytes in colon mucosa. Large numbers of IL-10-positive lymphocytes were observed in wild type mice both those with DSS induced colitis and untreated controls. Only sporadic IL-10 positivity was found in histamine-deficient mice. Significant differences were found in the composition of the fecal bacterial flora between the two groups. CONCLUSION: The reduced number of IL-10-positive lymphocytes in the intestinal mucosa of histamine-deficient, histidine decarboxylase knockout mice and the altered fecal bacterial flora in these animals suggest that histamine may play a role in the pathophysiology of inflammation in the colon of normal animals by upregulating local IL-10 production and stimulating a local shift to Th2 response.

Animals↗
PubMed1998

Diffuse lymphoplasmacytic acalculous cholecystitis: a distinctive form of chronic cholecystitis associated with primary sclerosing cholangitis.

Inflammation of the gallbladder is known to occur in patients with primary sclerosing cholangitis (PSC). However, the histological features of this form of cholecystitis have not been adequately defined. The aim of this study was to compare the inflammatory lesions of PSC-associated cholecystitis with those present in other cholecystopathies. The cases consisted of 11 gallbladders from patients with PSC who underwent liver transplantation. As controls, gallbladders from liver transplant patients with primary biliary cirrhosis (n = 4) and other chronic nonbiliary hepatopathies (n = 8), and 13 cholecystectomies from patients with chronic cholecystitis with (n = 10) and without (n = 3) lithiasis, were studied. The following histological features were tabulated on coded slides: presence, depth of involvement, and distribution of the inflammatory infiltrate, predominant cell type, presence of lymphoid aggregates, epithelial damage, metaplastic changes (pyloric or intestinal), fibrosis, smooth muscle hypertrophy, and presence of Rokitansky-Aschoff sinuses. At variance with the wide range of histological abnormalities present in other forms of chronic cholecystitis, most PSC-related cholecystitis showed a diffuse infiltrate (6 of 11) rich in plasma cells (6 of 11) predominantly confined to the lamina propria (9 of 11). The combination of these three features was present exclusively in PSC (5 of 11 PSC cholecystitis compared with 0 of 25 controls; P = .001). In conclusion, this study suggests that a characteristic form of cholecystitis may develop in patients with PSC.

Cholangitis, Sclerosing↗
PubMed2006

Implication of TNF-related apoptosis-inducing ligand in inflammatory intestinal epithelial lesions.

BACKGROUND & AIMS: Few data exist on the molecular events causing intestinal epithelial destruction during inflammatory processes, such as inflammatory bowel disease (IBD). In this work, we analyzed the potential implication of tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) in these inflammatory lesions. METHODS: TRAIL and TRAIL-receptor expression were analyzed in normal, inflammatory ileum/colon and human intestinal epithelial cell (IEC) lines (HIEC), Caco-2, and HT-29 using RNase protection assay, real-time and reverse-transcription polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blot analysis. TRAIL-induced activation of NF-kappaB was determined by electrophoretic mobility shift assay. Caspase-recruitment domain (CARD)15 expression and interleukin-(IL)8 production were studied by RT-PCR and enzyme-linked immunosorbent assay. Apoptosis was monitored using Annexin-V/caspase-3 assays. RESULTS: Normal mature IEC expressed low TRAIL levels, whereas, in inflammatory lesions, TRAIL messenger RNA and protein were markedly up-regulated in IEC and lamina propria lymphocytes at levels comparable with trinitrobenzene sulfonic acid-induced colitis. Interferon-gamma and TNF-alpha potently induced TRAIL in IEC. In vitro analyses revealed a dual biologic effect of TRAIL on HIEC: Under noninflammatory conditions, TRAIL up-regulated via nuclear factor-kappaB CARD15 and IL-8, whereas, under inflammatory conditions, TRAIL became a potent inducer of apoptosis in HIEC, which was confirmed ex vivo using ileal organ cultures. TNF-alpha markedly increased the expression of the proapoptotic receptor TRAIL-R2. TRAIL-induced IEC apoptosis required a functional caspase cascade. CONCLUSIONS: TRAIL is a new inflammatory mediator implicated in the homeostasis of intestinal epithelial barrier functions. TRAIL is highly up-regulated in IEC in inflammatory ileum and colon. It may augment in an auto-/paracrine fashion the elimination of IEC via apoptosis.

Animals↗
PubMed2006

Peroxisome proliferator activated receptor gamma in colonic epithelial cells protects against experimental inflammatory bowel disease.

INTRODUCTION: Peroxisome proliferator activated receptor gamma (PPARgamma) is expressed in epithelial cells, macrophage, and T and B lymphocytes. Ligand induced activation of PPARgamma was reported to attenuate colitis activity but it is not clear whether this protection is mediated by epithelial or leucocyte PPARgamma. METHODS: Mice with targeted disruption of the PPARgamma gene in intestinal epithelial cells, generated using a villin-Cre transgene and floxed PPARgamma allele and designated PPARgamma(DeltaIEpC), were compared with littermate mice having only the PPARgamma floxed allele with no Cre transgene that expressed PPARgamma in the gut, designated PPARgamma(F/F). Colitis was induced by administering dextran sodium sulphate (DSS) and the two mouse lines compared for typical symptoms of disease and expression of inflammatory cytokines. RESULTS: PPARgamma(DeltaIEpC) mice displayed reduced expression of the PPARgamma target genes ADRP and FABP in the gut but were otherwise normal. Increased susceptibility to DSS induced colitis, as defined by body weight loss, colon length, diarrhoea, bleeding score, and altered histology, was found in PPARgamma(DeltaIEpC) mice in comparison with PPARgamma(F/F) mice. Interleukin (IL)-6, IL-1beta, and tumour necrosis factor alpha mRNA levels in colons of PPARgamma(DeltaIEpC) mice treated with DSS were higher than in similarly treated PPARgamma(F/F) mice. The PPARgamma ligand rosiglitazone decreased the severity of DSS induced colitis and suppressed cytokine production in both PPARgamma(F/F) and PPARgamma(DeltaIEpC) mice. CONCLUSIONS: These studies reveal that PPARgamma expressed in the colonic epithelium has an endogenous role in protection against DSS induced colitis and that rosiglitazone may act through a PPARgamma independent pathway to suppress inflammation.

Animals↗
PubMed2002

Differential requirement for NF-kappa B family members in control of helminth infection and intestinal inflammation.

The NF-kappaB family of transcription factors is critical in controlling the expression of a wide range of immune response genes. However, whether individual family members perform specific roles in regulating immunity and inflammation remains unclear. Here we investigated the requirement for NF-kappaB1, NF-kappaB2, and c-Rel in the expression of Th2 cytokine responses, development of host protective immunity, and regulation of intestinal inflammation following infection with the gut-dwelling helminth parasite Trichuris muris. While mice deficient in c-Rel mounted sufficient Th2 responses to expel infection, NF-kappaB1 knockout (KO) and NF-kappaB2 KO mice developed chronic infections associated with elevated production of Ag-specific IFN-gamma. However, only infected NF-kappaB1 KO mice exhibited polarized IFN-gamma responses associated with the loss of intestinal goblet cells and the development of destructive colitis-like pathology. Furthermore, blockade of IL-12 (previously shown to confer resistance in susceptible strains) recovered Ag-specific IL-13 responses and resistance to infection in NF-kappaB2 KO, but not NF-kappaB1 KO mice. Therefore, unique infection, immunological, and pathological outcomes were observed in different NF-kappaB KO strains. Taken together, these results provide direct evidence of nonoverlapping functions for NF-kappaB family members in the development of Th2 cytokine-mediated resistance to T. muris and the control of infection-induced intestinal inflammation.

Animals↗
PubMed1986

In vitro IgE production by peripheral blood lymphocytes and rectal mucosal biopsies and antigen-induced basophil degranulation in patients with inflammatory bowel disease.

IgE production by peripheral blood lymphocytes (PBL) and rectal mucosal biopsies in vitro has been examined in patients with ulcerative colitis (UC) and Crohn's disease (CD). The degranulation of peripheral blood basophils to food antigens has also been investigated in these patients. Mitogen-induced IgE production was reduced in patients with UC, but enhanced in PBL cultures from patients with CD. Increased numbers of basophils degranulated in the presence of cows' milk in UC patients, but normal responses occurred in patients with CD. This evidence supports the suggested role of IgE-mediated mechanisms involving mast cell/basophil interactions in the pathogenesis of inflammatory bowel disease.

Antigens↗