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At least 451 records · Page 25Linked to original sources
PubMed1999

Tumour necrosis factor-alpha (TNF-alpha) transcription and translation in the CD4+ T cell-transplanted scid mouse model of colitis.

The adoptive transfer of activated CD4+ alpha/beta T cell blasts from the spleens of immunocompetent C.B-17+/+ or BALB/cdm2 mice into C.B-17scid/scid (scid) mice induces a colitis in the scid recipient within 8 weeks, which progresses to severe disease within 16 weeks. T cells isolated from recipient colon show a Th1 cytokine phenotype. We have examined the relationship between the phenotype of the cellular infiltrate and the transcription and translation of the proinflammatory cytokine TNF-alpha. The techniques of double indirect immunohistology and in situ hybridization using digoxigenin-labelled riboprobes were used. The prominent myeloid cell infiltrate in diseased tissues comprised F4/80+, Mac-l+ macrophages, neutrophils, dendritic cells and activated macrophages. TNF-alpha transcription and translation were associated with activated macrophages in the lamina propria. Activated macrophages transcribing and translating TNF-alpha were clustered in areas of tissue destruction. Crypt epithelium of inflamed tissues transcribed TNF-alpha at a very early stage of the disease process, but translation of TNF-alpha protein could only be found in advanced epithelial dysplasia. This indicates differential post-transcriptional control of TNF-alpha in activated macrophages and the epithelium.

Adoptive Transfer↗
PubMed2002

Interleukin-2-Deficient mice: effect on cytokines and inflammatory cells in chronic colonic disease.

Mice deficient in interleukin-2 (IL-2-/-) develop inflammatory bowel disease resembling human ulcerative colitis. After death, macroscopic and microscopic scores were used to determine colonic inflammation. Both scores were significantly increased in the colon of IL-2-/- mice as compared to wild types mice. The level of IL-1beta 24-week-old was increased in IL-2-/- mice produced by the colon as compared with IL-2+/+ controls. However, the concentrations of IL-6 and IL-10 were not changed. The spleen weight of IL-2-/- mice was significantly increased compared with IL-2+/+ controls. We used immunochemical techniques in low-temperature paraffin-embedded spleen of IL-2-/- mice to examine pathological changes of CD4+ T cells, CD8' T cells, and CD11b+ cells. The tissue was successfully stained and was well preserved. The percentage CD4+ T cells was not significantly changed, while the percentage CD8+ T cells was significantly decreased in IL-2-/- mice compared with IL-2+/+ controls. On the other hand, the percentage CD11b+ cells was significantly increased in the spleen of IL-2-/- mice compared with IL-2+/- controls. As well as the marked difference in CD8+ and CD11b+ cells in the spleen, the increased level of IL-1beta in colonic tissue might indicate that cytotoxic T cells as well as macrophages are involved in the development and/or perpetuation of the inflammatory reactions in IL-2-/- mice.

Animals↗
PubMed2007

Extracorporeal elimination of TNF-alpha-producing CD14(dull)CD16(+) monocytes in leukocytapheresis therapy for ulcerative colitis.

BACKGROUND: In recent years leukocytapheresis using a leukocyte removal filter (known as lymphocytapheresis, LCAP) has been applied to the treatment of various autoimmune diseases including ulcerative colitis (UC). In the present study we aimed to clarify how LCAP therapy modifies inflammatory responses by modulating circulating TNF-alpha-producing monocytes. METHODS: Mononuclear cells were obtained from blood before and after the first treatment, and the expression profiles of various immune cells (naive versus. memory, regulatory CD4(+)CD25(bright) versus non-regulatory CD4(+)CD25(-) T cells, and CD14(+)CD16(-) versus CD14(dull)CD16(+) monocytes) were assessed. To evaluate immunological differences between CD14(+)CD16(-) and CD14(dull)CD16(+) monocytes, the expression of TNF-alpha, IL-6, IL-12, IL-10, IL-18, surface toll-like receptor 2 (TLR2), TLR4, and other activation markers including HLA-DR, CD80 and CD86, as well as cytokine profiles, were analyzed. RESULTS: LCAP treatment selectively removed CD14(dull)CD16(+) monocytes, which preferentially produce TNF-alpha and IL-12 and express HLA-DR, CD80, CD86, and TLR2, compared with the major fraction of CD14(+)CD16(-) monocytes, which conversely produce a higher amount of IL-10. In addition, the CD4(+)CD45RO(+)CD62L(-)/CD4(+)CD45RO(+)CD62L(+) ratio was significantly lower after LCAP therapy. However, the CD4(+)CD25(bright)/total CD4(+) ratio did not change. CONCLUSIONS: The present findings revealed the real target of proinflammatory CD14(dull)CD16(+) monocytes removed during LCAP treatment of UC and that LCAP might be used as an extracorporeal anti-TNF-alpha therapy, expanding the clinical applications of this procedure to include the treatment of Crohn's disease.

Adult↗
PubMed2001

Prevalence of an ulcerative colitis-associated CD8+ T cell receptor beta-chain CDR3-region motif and its association with disease activity.

The normal human intestinal mucosa contains clonal T cell expansions. Clonal populations of T cells can be determined through evaluation of the idiotypic, hypervariable region of their T cell receptor (TCR). We have previously reported that there exists a highly conserved TCR pattern among intestinal CD8+ T cells in the majority of ulcerative colitis (UC) patients undergoing colectomy that was not present in normal control individuals. This TCR pattern, or motif, was characterized by particular beta-chain usage (TCRBV3 and TCRBJ1S6) and a defined length in the hypervariable third complementarity determining region (CDR3). The aim of this study was to assess the motif's relationship to disease activity. Subjects were 66 with UC, 19 with Crohn's disease, 14 inflammatory controls, and 6 normal controls. cDNA and gDNA were prepared from colonic biopsies and paraffin blocks, respectively, obtained from study subjects and used to assess TCRBV CDR3 region length and usage, as well as for cloning and sequencing of TCRs. The TCRBV CDR3 region was present in 25 of a series of 48 UC subjects but only 3 of 19 Crohn's disease patients and 3 of 14 inflammatory controls. The motif was more common in UC than either Crohn' s disease or inflammatory controls (chi2 = 7.5, P = 0.006, and chi2 = 4.1, P = 0.04, respectively). The motifs presence was not dependent upon histologic disease activity (either active or inactive UC). Clinical UC disease activity was also not significantly associated with an increased presence of the motif in 14 paired biopsies, which were taken during times of clinical activity or inactivity. There was a trend toward persistence of the motif, as it was present in 6 of 14 subjects over a 3- to 6-month time period. The previously described UC-associated TCRBV CDR3 region motif located in the intestinal CD8+ T-cell subset is found in a significant proportion of UC subjects. The TCR motif does not significantly discriminate active from inactive disease states. The persistent and diffuse nature of this TCR-associated motif in UC suggests that an ongoing T-cell response to a particular antigen(s) is occuring in this disorder.

Amino Acid Sequence↗
PubMed2003

Expression of lymphotoxin-beta (LT-beta) in chronic inflammatory conditions.

Functional studies in gene-knockout and transgenic mice systems have shown that lymphotoxin-alpha and lymphotoxin-beta (LT-alpha and LT-beta) are of fundamental importance in peripheral lymphoid organ development, but it remains unclear what role these cytokines have to play in the adult immune response and in the pathogenesis of disease. In this study, a polyclonal anti-serum to human LT-beta was used to investigate the distribution of LT-beta by immunohistochemistry in normal and diseased tissues. In the gut, lymph nodes, spleen, and tonsil, there was some LT-beta present on a variety of lymphoid cell types. In contrast, strong staining for LT-beta was observed on plasma cells and a subpopulation of CD4+ T cells in tissues affected by chronic inflammatory disease or infection, for example in inflammatory bowel disease, and in lymph nodes obtained from patients with sarcoidosis and tuberculosis. In tuberculous and sarcoid lymph nodes, LT-beta expression also occurred on some but not all epithelioid histiocytes within granulomas and on multi-nucleated giant cells. These findings support a role for LT-beta in human disease and suggest that it might represent a therapeutic target in a variety of common infective or inflammatory disorders.

Adult↗
PubMed1983

The classification of feline colitis.

Clinical and pathological features of a variety of forms of feline colitis or enterocolitis were examined and classified into 9 separate entities: Salmonella enterocolitis, the colitis of feline infectious peritonitis, mycotic enterocolitis, acute angiopathic colitis, acute angiopathic colitis with ischaemic ulcers, feline granulomatous colitis, the colitis of feline panleucopenia, feline histiocytic colitis, and feline ulcerative, lymphocytic mucosal-submucosal colitis.

Animals↗
PubMed1997

CD45RBhigh CD4+ T cells from IFN-gamma knockout mice do not induce wasting disease.

Transfer of CD45RBhigh CD4+ T cells from normal mice to congenic SCID mice induces wasting disease, a murine model of inflammatory bowel disease. In this model, colonic inflammation is considered to be caused by a disregulated Th1 response, and Th1 cytokines, especially IFN-gamma, have been suggested to play an important role in the pathogenesis of wasting disease. In order to elucidate the potential role of IFN-gamma in the pathogenesis of wasting disease, we transferred CD45RBhigh CD4+ T cells from IFN-gamma knockout (GKO) mice to congenic SCID mice. The recipient mice were absolutely free of symptoms and clinical signs of disease and showed body-weight gain similar to that seen in normal mice. These data demonstrate the essential and non-redundant role of IFN-gamma in the pathogenesis of wasting disease.

Animals↗
PubMedDate not supplied

Microscopic colitis: pathologic considerations, changing dogma.

Microscopic colitis as an entity was first recognized in 1976, and has become one of the most frequent diseases to exclude on colonic mucosal biopsies. In some pathology practices, up to 30% of colonic biopsies received are from patients in whom microscopic colitis is the clinical question. In this review, the evolution of the terminology and early studies describing the pathology of microscopic colitis are discussed. The pathology of lymphocytic and collagenous colitis is reviewed in detail, including common diagnostic pitfalls, and what is currently known about the pathogenesis of these diseases. The differential diagnosis of microscopic colitis includes other idiopathic inflammatory bowel diseases (Crohn's and ulcerative colitis), infections, and drug reactions. The distinction between these entities and microscopic colitis is discussed in detail. Finally, recent studies have revealed new histopathologic changes in microscopic colitis that challenge the currently held concepts of how microscopic colitis fits into the spectrum of inflammatory bowel diseases.

Colitis↗
PubMed2005

Mu opioid receptor expression is increased in inflammatory bowel diseases: implications for homeostatic intestinal inflammation.

BACKGROUND AND AIMS: Recent studies with mu opioid receptor (MOR) deficient mice support a physiological anti-inflammatory effect of MOR at the colon interface. To better understand the potential pharmacological effect of certain opiates in inflammatory bowel diseases (IBD), we (1) evaluated the regulation in vivo and in vitro of human MOR expression by inflammation; and (2) tested the potential anti-inflammatory function of a specific opiate (DALDA) in inflamed and resting human mucosa. PATIENTS AND METHODS: Expression of MOR mRNA and protein was evaluated in healthy and inflamed small bowel and colonic tissues, isolated peripheral blood mononuclear cells and purified monocytes, and CD4+ and CD8+ T cells from healthy donors and IBD patients. The effect of cytokines and nuclear factor kappaB (NFkappaB) activation on MOR expression in lymphocyte T and monocytic human cell lines was assessed. Finally, DALDA induced anti-inflammatory effect was investigated in mucosal explants from controls and IBD patients. RESULTS: MOR was expressed in ileal and colonic enteric neurones as well as in immunocytes such as myeloid cells and CD4+ and CD8+ T cells. Overexpressed in active IBD mucosa, MOR was significantly enhanced by cytokines and repressed by NFkappaB inhibitor in myeloid and lymphocytic cell lines. Furthermore, ex vivo DALDA treatment dampened tumour necrosis factor alpha mRNA expression in the colon of active IBD patients. CONCLUSIONS: Given the increased expression of MOR and the ex vivo beneficial effect of DALDA in active IBD, natural and/or synthetic opioid agonists could help to prevent overt pathological intestinal inflammation.

Adult↗
PubMed1980

A therapeutic trial of anti-lymphocytic globulin in acute ulcerative colitis.

The results of the preliminary part of a controlled therapeutic trial of antilymphocytic globulin (ALG) in severe acute ulcerative colitis are presented. 10 patients have been studied in this part of the trial, 5 receiving standard treatment with corticosteroids, and 5 receiving ALG, in a dose of 1 g daily for 5 days, in addition to the standard treatment. No difference has been observed in the clinical course of the patients in the two groups. A continuation of the trial is in progress, using ALG in a larger dose (2 g daily for 5 days).

Acute Disease↗
PubMed2005

CD18 is required for optimal development and function of CD4+CD25+ T regulatory cells.

CD4+CD25+ T regulatory (Treg) cells inhibit immunopathology and autoimmune disease in vivo. CD4+CD25+ Treg cells' capacity to inhibit conventional T cells in vitro is dependent upon cell-cell contact; however, the cell surface molecules mediating this cell:cell contact have not yet been identified. LFA-1 (CD11a/CD18) is an adhesion molecule that plays an established role in T cell-mediated cell contact and in T cell activation. Although expressed at high levels on murine CD4+CD25+ Treg cells, the role of LFA-1 in these cells has not been defined previously. We hypothesized that LFA-1 may play a role in murine CD4+CD25+ Treg function. To evaluate this, we analyzed LFA-1-deficient (CD18-/-) CD4+CD25+ T cells. We show that CD18-/- mice demonstrate a propensity to autoimmunity. Absence of CD18 led to diminished CD4+CD25+ T cell numbers and affected both thymic and peripheral development of these cells. LFA-1-deficient CD4+CD25+ T cells were deficient in mediating suppression in vitro and in mediating protection from colitis induced by the transfer of CD4+CD25- T cells into lymphopenic hosts. Therefore, we define a crucial role for CD18 in optimal CD4+CD25+ Treg development and function.

Animals↗
PubMed1986

Raised serum levels of IgM-rheumatoid factor and anti-F(ab')2 autoantibodies in patients with active inflammatory bowel disease.

The serum levels of IgM-Rheumatoid Factor and of anti-F(ab')2 autoantibodies were investigated in patients with inflammatory Bowel Disease (IBD) by sensitive radioimmunoassays. Serum levels of the 2 autoantibodies were significantly increased in active IBD. In patients with Crohn's Disease raised titers of the 2 antibodies appeared to be also related to colonic involvement. There was, in Crohn's Disease, a significant association between concordantly positive results with the 2 assays and the occurrence of systemic complications. Immunocomplexes detected by the C1q-SP method were higher in sera of Crohn's Disease patients with raised IgM-RF than in the others. Data from the present investigation indicate that in active IBD and particularly in Crohn's Disease autoantibodies directed against different parts of the immunoglobulin molecule may be produced. These findings add support to the concept that an in vivo polyclonal B-cell activation may occur in these patients.

Adult↗
PubMed1997

Colonic nitrite and immunoglobulin G concentrations in dogs with inflammatory bowel disease.

OBJECTIVE: To evaluate lavage analytes as markers of mucosal inflammation in healthy dogs and dogs with inflammatory bowel disease (IBD). DESIGN: Case control study. ANIMALS: 9 healthy dogs and 10 dogs with IBD. PROCEDURE: A polyethylene glycol electrolyte solution was administered into the dogs colons via a rectal balloon catheter prior to colonoscopy. Lavage solution was allowed to remain intraluminally for 30 minutes and then was withdrawn. Lavage supernatant samples were immediately analyzed for total protein, IgG, and nitrite concentrations and myeloperoxidase activity. Mucosal biopsy specimens were obtained from the descending colon and histologically reviewed. RESULTS: All dogs with IBD had mild to severe lymphocytic-plasmacytic colitis, whereas 8 of 9 healthy dogs did not have substantial mucosal inflammation. Myeloperoxidase activity was not detected in lavage samples from healthy dogs or dogs with IBD. Total protein concentration was not significantly different between groups. Mean nitrite and IgG concentrations were significantly higher in samples from dogs with IBD (1.83 nmol/ml and 46 mg/dl, respectively), compared with samples from healthy dogs (0.245 nmol/ml and undetectable concentrations, respectively). Severity of lesions was not correlated with nitrite or IgG concentration. CLINICAL IMPLICATIONS: Assay of nitrite and IgG concentrations in colonic lavage fluid is a simple, objective means of evaluating mucosal inflammation in dogs with IBD. Potential uses include monitoring response to treatment and evaluation of complex cases of chronic intestinal inflammation.

Analysis of Variance↗