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At least 1,279 records · Page 71Linked to original sources
PubMed2006

Cytokine tumor necrosis factor-alpha A promoter gene polymorphism at position -308 G-->A and pediatric inflammatory bowel disease: implications in ulcerative colitis and Crohn's disease.

OBJECTIVES: Our pilot study aimed to determine the effect of tumor necrosis factor-alpha (TNF-alpha) 308 G-->A promoter single-nucleotide polymorphism in pediatric inflammatory bowel disease (IBD), its influence on inflammatory activity and the clinical manifestations. METHODS: We obtained genomic DNA from 164 subjects, 82 with long-standing IBD aged 8 to 18 years: 46 with Crohn disease (CD) and 36 with ulcerative colitis (UC). Eighty-two healthy children served as the control population. Genotyping was determined by using a restriction enzyme-based assay. TNF-alpha 308 G-->A polymorphism was assessed in terms of inflammatory (C-reactive protein [CRP]) and disease activity. The latter was assessed by the Pediatric Crohn's Disease Activity Index (PCDAI) and the Truelove index for CD and UC, respectively. RESULTS: Significant differences in TNF-alpha 308 A polymorphism were found between the IBD group and controls (P < 0.05) and the UC group and controls (P < 0.001). No differences were noted between TNF-alpha 308 A polymorphism and clinical characteristics in UC. The frequency of the -308 A allele of TNF was not different in CD compared with that in the control group. The frequency of TNF-alpha 308 A genotype was significantly higher in CD patients with predominantly stenosing/penetrating disease compared with patients without complications (P < 0.001) and healthy controls (P < 0.01). In CD patients, those carrying TNF -308 A had a significant increase in CRP (P < 0.05) and the PCDAI (P < 0.05). In CD, CRP levels strongly correlated with the PCDAI (r = 0.6150, P < 0.001). In UC, significant differences among the mean levels of CRP (P < 0.05) and disease activity (P < 0.001) related to TNF-alpha 308 A polymorphism were found. Allele distribution (odds ratio, 12.9; CI, 1.18-140.81, P < 0.001) and CRP serum levels (odds ratio, 1.020; CI, 1.00-1.04, P < 0.001) were independently associated with CD complications. CONCLUSIONS: Although not necessarily dictating IBD initiation, the TNF-alpha 308 A polymorphism may play a role in modifying the CD phenotype. The polymorphism may influence disease activity as well as more intense inflammatory activity in both forms of IBD and may modify the progression of chronic digestive tract inflammation.

Adolescent↗
PubMed2004

The clinical significance of focally enhanced gastritis.

Focally enhanced gastritis (FEG) is typified by small collections of lymphocytes and histiocytes surrounding a small group of foveolae or gastric glands, often with infiltrates of neutrophils. Several studies have found that FEG is commonly seen in Crohn's disease patients with a positive predictive value of 94%. Additional studies have found that FEG is present in up to 20% of pediatric ulcerative colitis patients, suggesting that FEG is a marker for inflammatory bowel disease (IBD) in general. We reviewed all gastric biopsies from a single calendar year (1999) to study the incidence of FEG and its relationship to IBD. A total of 34 cases of FEG were found among 971 gastric biopsies from 927 patients. Only 4 FEG patients were found to have IBD (2 Crohn's, 1 ulcerative colitis and 1 chronic colitis, type indeterminate, 11.8%, positive predictive value of 5.9%). Five FEG patients were status post bone marrow transplantation (14.7%). There were no other clinical correlations and gastric histopathology did not predict which patients with FEG had IBD. We conclude that FEG is not a common histologic finding in our patient population and that the positive predictive value of this finding is much too low to be thought of as a specific marker for IBD. An isolated biopsy diagnosis of FEG should not be interpreted as being suggestive of Crohn's disease.

Adult↗
PubMedDate not supplied

Impact of depressive mood on relapse in patients with inflammatory bowel disease: a prospective 18-month follow-up study.

OBJECTIVE: There is evidence of an interaction between psychological factors and activity of inflammatory bowel disease (IBD). We examined the influence of depressive mood and associated anxiety on the course of IBD over a period of 18 months in a cohort of patients after an episode of active disease. METHODS: In this prospective, longitudinal, observational study, 60 patients (37 women and 23 men) with clinically inactive IBD (Crohn disease, n = 47, 78%; ulcerative colitis, n = 13, 22%) were enrolled after a flare of disease. Psychological status, health-related quality of life (HRQOL), and disease activity were evaluated at baseline and then every 3 months for a period of 18 months by means of clinical and biological parameters, the Beck Depression Inventory (BDI), the Spielberger State-Trait Anxiety Inventory, the Inflammatory Bowel Disease Questionnaire, the Perceived Stress Questionnaire, and the Rating Form of Inflammatory Bowel Disease Patients Concerns. RESULTS: At baseline, depression (BDI > or = 13 points) was found in 17 of 60 (28%) patients. Thirty-two patients (59%) experienced at least one relapse during the 18 months of follow-up. Regression analysis showed a significant correlation between BDI scores at baseline and the total number of relapses after 12 (p <.01) and 18 months (p <.01) of follow-up. Furthermore, depression scores at baseline correlated with the time until the first recurrence of the disease (p <.05). Anxiety and low HRQOL were also related with more frequent relapses during follow-up (p <.05 and p <.01, respectively). CONCLUSIONS: Psychological factors such as a depressive mood associated with anxiety and impaired HRQOL may exert a negative influence on the course of IBD. Therefore, assessment and management of psychological distress should be included in clinical treatment of patients with IBD.

Adult↗
PubMed2026

The complement system in inflammatory bowel disease: from early observations to emerging frontiers.

PURPOSE OF REVIEW: The complement system is one of the most evolutionarily conserved arms of innate immunity and has re-emerged as an important regulator of intestinal inflammation in inflammatory bowel disease (IBD). Early observations from the mid-1970&#x200a;s such as complement deposition in diseased bowel tissue and elevated serum complement levels in patients with ulcerative colitis and Crohn's disease have evolved into a nuanced understanding of how individual complement components can exert both protective and pathogenic effects in IBD. This review highlights recent advances in complement biology and examines how complement shapes intestinal immune responses, particularly in the setting of ongoing inflammation. RECENT FINDINGS: The complement system consists of more than 60 proteins that act as rapid first responders to infection. Although traditionally considered primarily liver-derived circulating effectors, recent work has demonstrated local synthesis and activation of key complement components at mucosal sites, including the colon. In parallel, genome-wide association studies have identified variants in complement genes associated with severe IBD complications. Collectively, these findings reveal a dichotomous role for complement in IBD, whereby excessive activation promotes inflammation, while impaired function compromises host defense and worsens disease outcomes. SUMMARY: Complement-targeted therapies have been effective in other diseases but have not yet translated to IBD. A deeper understanding of context-dependent protective versus pathogenic complement functions will be essential for developing future therapeutic strategies.

Humans↗
PubMed2004

Infection with cytomegalovirus in patients with inflammatory bowel disease: prevalence, clinical significance and outcome.

Despite frequent use of immunosuppressive drugs in patients with inflammatory bowel disease (IBD) and reports of cytomegalovirus (CMV) infection following post-transplant immunosuppression, data on the frequency and clinical significance of CMV in patients with IBD are scant. Sixty-three patients with IBD (61 ulcerative colitis and two Crohn's disease) were evaluated for CMV using serology (IgM antibody, mu-capture ELISA), PCR for CMV DNA in colonic biopsy and histological assessment of haematoxylin and eosin-stained colonic biopsy. Positive result in any test was considered as CMV infection. Various parameters associated with CMV infection were analysed using univariate and multivariate analysis. Ten of 63 (15.8 %) patients (age 36.0 +/- 11.2 years, 31 female) were infected with CMV (DNA alone in four, IgM antibody alone in two and both in four, inclusion body in one). Patients with CMV infection were more often female (8/10 vs 23/53, P < 0.05), had pancolitis (10/10 vs 33/53, P < 0.05), histological activity (9/10 vs 17/53, P < 0.005) and used azathioprine (5/10 vs 7/53, P = 0.04; Fisher exact test for all). On multivariate analysis, female gender, pancolitis and histological activity were the independent factors associated with infection. Patients with CMV infection more often required surgical treatment for IBD (4/10 vs 4/53, P = 0.01) and had fatal outcome (3/10 vs 0/53, P = 0.003). CMV infection in patients with IBD may be common and is associated with poor outcome. PCR of rectal biopsy was the most sensitive method of detection followed by IgM antibody for diagnosis.

Adolescent↗
PubMed2005

Tumor necrosis factor family members and inflammatory bowel disease.

Tumor necrosis factor (TNF) is one of the most potent effector cytokines in the pathogenesis of inflammatory bowel disease (IBD). Previous studies strongly implicate the critical involvement of several TNF family members in human IBD. This review focuses on the recent studies of TNF family members in IBD development. In particular, we discuss the findings about LIGHT (homologous to lymphotoxins, inducible expression, competes with herpes simplex virus glycoprotein D for herpes viral entry mediator, a receptor expressed on T lymphocytes) in the pathogenesis of IBD, and the potential mechanisms by which LIGHT induces IBD. Such mechanisms may also apply to other TNF family members.

Animals↗
PubMed2004

Enamel matrix proteins in the treatment of intra-bony defects. A prospective 24-month clinical trial.

BACKGROUND: A growing flow of recent evidence indicates enamel matrix derivative (EMD, Emdogain) as a useful tool for the regeneration of periodontal tissues. This prospective clinical study aimed to evaluate the efficacy of EMD combined with surgical treatment of periodontal intra-bony defects, as compared with surgery alone, up to 24 months of follow-up. METHODS: Twenty-four intra-bony defects were treated in 24 patients in a single clinical centre. Each defect had intra-bony depth (IBD) > or = 4 mm and probing pocket depth (PPD) > or = 6 mm. Patients were randomly assigned to either test or control group. Plaque index (PI), gingival index (GI), PPD and periodontal attachment level (PAL) were assessed at baseline pre-surgical examination at the site to be treated. Full mouth plaque score (FMPS) and full mouth bleeding score (FMBS) were also evaluated. Twelve patients were treated by simplified papilla preservation flap technique (control group), while 12 patients were treated with the same surgical technique plus EMD after ethylenediamine tetraacetic acid root conditioning (test group). Any probing at the involved sites was avoided in the first year post-surgery. Radiographs were taken at baseline, 12 and 24 months after surgery using customized bite blocks. Intra-bony defect depth (IBD) and angle (IBA) were measured from X-rays by a computer-aided technique. At 12 and 24 months post-surgery, FMPS, FMBS, PI, GI, PPD, PAL and radiographic IBD and IBA were assessed. The difference between each follow-up and baseline, and between groups at each follow-up was evaluated for the above parameters by standard statistical methods. RESULTS: In both groups, clinical and radiographic parameters were improved at either 12 or 24 months when compared with baseline. The test group displayed better outcomes when compared with the control group for IBD, PPD, and PAL gain at 12 months, and only for PAL and IBD gain at 24 months. No adverse event related to the use of EMD was reported. CONCLUSIONS: The surgical procedure used in the present study, aiming for maximum preservation of the regenerative potential of periodontal tissues, showed per se excellent results. The use of EMD as an adjunct to periodontal surgery in the treatment of angular defects possibly enhances periodontal regeneration rate.

Adult↗
PubMed1997

Review article: In vitro models in inflammatory bowel disease research--a critical review.

Research efforts in inflammatory bowel disease (IBD) have been directed towards the epithelium as it has become clear that epithelial cells play a critical role in inflammatory response. Most research involving IBD employs in vitro techniques. In vitro epithelial cell studies have played and are continuing to play a major role in providing specific information relevant to IBD. Thus, such studies have provided irrefutable evidence that epithelial responses can be induced by microbes/microbial products and by immune activation. Culture experiments have provided insights into the effects of individual cytokines and other inflammatory mediators on epithelial pathophysiology, injury and repair, apoptosis, necrosis, and other processes that may be involved in IBD. Activated epithelial cells can participate in and even orchestrate immune responses, by stimulating T cells (and possibly others) and by producing cytokines that recruit specific inflammatory cells. Physiological regulation of epithelial tight junctions has been demonstrated by in vitro studies; the implication of this information for treating IBD is just beginning to be explored. It is becoming increasingly clear that epithelial processing and presentation of antigens is critical to the outcome of the immune response.

Animals↗
PubMed1992

IL-2 production by intestinal lamina propria cells in normal inflamed and cancer-bearing colons.

Biologically significant levels of IL-2 activity were produced by isolated lamina propria mononuclear cells (LPMC) from normal intestine (n = 12), cancer-bearing colons (n = 35) and inflammatory bowel disease (IBD) affected tissue (n = 12). The levels of IL-2 produced were similar for all three sources of LPMC (normal 252 +/- 48 U/ml, IBD-affected mucosa 197 +/- 42 U/ml and colon cancer 285 +/- 43 U/ml). These levels were significantly greater than those produced by peripheral blood mononuclear cells (20 +/- 5 U/ml, P less than 0.01) on a per cell basis. In mucosa from cancer-bearing colons the amount of IL-2 produced by LPMC was unaffected by the invasiveness of the colon cancer. LPMC IL-2 production was markedly suppressed by drugs used in IBD therapy. 5-Aminosalicylic acid (5-ASA) reduced activity in a dose-dependent fashion. At a dose equivalent to the faecal therapeutic level of 0.5 mg/ml activity, IL-2 production by LPMC was suppressed to 3.4% of controls. Similarly, exposure of LPMC to cyclosporin A (CyA) and hydrocortisone (HC) at therapeutic levels reduced IL-2 activity to less than 1% of controls. The major producers of IL-2 activity were shown to be CD3+ T lymphocytes and those bearing the activation markers IL-2R and TFR. Suppression of mucosal IL-2 production represents an important therapeutic mechanism of drugs used in the management of IBD including HC, 5-ASA and CyA. These results suggest that mucosal T cells produce appreciable levels of IL-2 activity that may be important in maintaining immune homeostasis in the normal intestine, provide anti-neoplastic cytotoxic activity and contribute to the inflammatory events that characterize the mucosal lesions of IBD.

Aminosalicylic Acids↗
PubMed1992

Absence of circulating interferon in patients with inflammatory bowel disease. Suggestion against an autoimmune etiology.

Whether inflammatory bowel diseases (IBD) can be classified as autoimmune disorders is not established. Since circulating acid-labile interferon-alpha (IFN-alpha) is believed to reflect autoimmune reactions, we tested sera from two groups of IBD patients for the presence of circulating IFN. No detectable IFN was found in 51 serum samples of IBD patients. Furthermore, in no serum sample of IBD patients were neutralizing anti-IFN antibodies found. In contrast, acid-labile IFN-alpha was present in sera from 21/52 HIV-infected and from 6/14 systemic lupus erythematosus patients. These observations provide evidence that IBD differs from systemic autoimmune disorders, at least for the presence of circulating IFN.

Autoantibodies↗
PubMed2004

Cathepsin D is up-regulated in inflammatory bowel disease macrophages.

Down-regulation of receptors involved in the recognition or transmission of inflammatory signals and a reduced responsiveness support the concept that macrophages are 'desensitized' during their differentiation in the intestinal mucosa. During inflammatory bowel disease (IBD) intestinal macrophages (IMACs) change to a reactive or 'aggressive' type. After having established a method of isolation and purification of IMACs, message for cathepsin D was one of the mRNAs we found to be up-regulated in a subtractive hybridization of Crohn's disease (CD) macrophages versus IMACs from control mucosa. The expression of cathepsin D in intestinal mucosa was analysed by immunohistochemistry in biopsies from IBD and control patients and in a mouse model of dextran sulphate sodium (DSS)-induced acute and chronic colitis. IMACs were isolated and purified from normal and inflamed mucosa by immunomagnetic beads armed with a CD33 antibody. RT-PCR was performed for cathepsin D mRNA. Results were confirmed by Northern blot and flow cytometrical analysis. Immunohistochemistry revealed a significant increase in the cathepsin D protein expression in inflamed intestinal mucosa from IBD patients compared to non-inflamed mucosa. No cathepsin D polymerase chain reaction (PCR) product could be obtained with mRNA from CD33-positive IMACs from normal mucosa. Reverse transcription (RT)-PCR showed an induction of mRNA for cathepsin D in purified IMACs from IBD patients. Northern blot and flow cytometry analysis confirmed these results. Cathepsin D protein was also found in intestinal mucosa in acute and chronic DSS-colitis but was absent in normal mucosa. This study shows that expression of cathepsin D is induced in inflammation-associated IMACs. The presence of cathepsin D might contribute to the mucosal damage in IBD.

Acute Disease↗
PubMed2006

Cathepsins B, L and D in inflammatory bowel disease macrophages and potential therapeutic effects of cathepsin inhibition in vivo.

The cathepsins D (CTSD), B (CTSB) and L (CTSL) are important for the intracellular degradation of proteins. Increased cathepsin expression is associated with inflammatory diseases. We have shown previously an induction of CTSD expression in intestinal macrophages (IMAC) in inflamed mucosa of patients with inflammatory bowel disease (IBD). Here we investigated the regulation of CTSB and CTSL in IMAC during IBD and effects of CTSD and CTSB/CTSL inhibition in vivo. Human IMAC were isolated from normal and inflamed mucosa. Reverse transcription-polymerase chain reaction (RT-PCR) was performed for CTSB and CTSL mRNA. Immunostaining was used to confirm PCR results. Cathepsin inhibition was investigated in the dextran-sulphate-sodium (DSS) colitis model in mice with application of pepstatin A (CTSD inhibitor), CA-074 (CTSB inhibitor) and Z-Phe-Tyr-aldehyde (CTSL inhibitor). CTSL mRNA was significantly up-regulated in IMAC isolated from IBD mucosa. Up-regulated protein expression was found mainly in areas of mucosal damage by immunostaining. Inhibition of CTSD in mouse DSS colitis was followed by an amelioration of the disease. Inhibitor-treated mice showed a significant lower histological score (HS) and less colon reduction in comparison to controls. Similarly, simultaneous inhibition of CTSB/CTSL was followed by a significant amelioration of colitis. Expression of tissue-degrading cathepsins is increased in IMAC in IBD. Inhibition of CTSD as well as CTSB/CTSL is followed by an amelioration of experimental colitis. The prevention of mucosal damage by cathepsin inhibition could represent a new approach for the therapy of IBD.

Animals↗
PubMed1987

Inflammatory bowel disease: effects on lifestyle.

While there has been speculation in the literature about what life with inflammatory bowel disease (IBD) is like, patients have not, prior to this study, been asked about their perceptions. This paper reports the results of a study which measured the impact of having IBD on eight lifestyle variables. Eighty IBD patients completed the Inflammatory Bowel Disease Stress Index. Results showed that although the impact of IBD on relationships, school and employment, recreational activities, sexuality, psychosomatic symptomatology, body image and worry was minimal, the patients' satisfaction with life was impaired as a result of having IBD. Rationale for this discrepancy and the significance of the findings for nurses are presented.

Adolescent↗
PubMed2006

Correlates of genetic differentiation and isolation by distance in 17 congeneric Silene species.

The contemporary pattern of intraspecific genetic variation can indicate the relative role of gene flow and local differentiation in shaping the evolutionary history and future trajectory of a species. To assess the recent influence of contrasting life history and demographic characteristics on genetic structure within a group of closely related species, patterns of genetic differentiation (F(ST) and related statistics) and isolation by distance (IBD) were compared among 17 congeneric herbaceous plant species. Data came from 35 published studies of 16 species, and a previously unpublished analysis of chloroplast genetic variation in the rare endemic Silene rotundifolia. Among-population genetic variance was most strongly influenced by the type of genetic marker used; cytoplasmic markers showed larger values than allozyme and anonymous nuclear markers. Other independently significant factors were geographical range size and, for allozyme studies, reproductive system; in particular, endemism and hermaphroditism were associated with higher among-population genetic variance, whereas large native geographical range and dioecy were associated with lower among-population variance. Over equivalent spatial scales, dioecious populations also showed weaker IBD than hermaphrodites, perhaps because increased population transience and/or variance in the spatial pattern of gene flow are more closely associated with dioecy in this genus. Invasive populations had both highly variable among-population genetic variance, and no evidence for IBD, consistent with nonequilibrium conditions. Other analysed factors including predominant pollinator had no discernable influence on genetic structure or patterns of IBD. In general, this comparative approach appears to be valuable for synthesizing the complementary information provided by F-statistics and IBD, and for indicating the relative importance of particular biological factors in shaping genetic variation within different species of a closely related plant group.

DNA, Chloroplast↗
PubMed2006

Genetics of recent habitat contraction and reduction in population size: does isolation by distance matter?

Fragmentation and loss of natural habitats are recognized as major threats to contemporary flora and fauna. Detecting past or current reductions in population size is therefore a major aim in conservation genetics. Statistical methods developed to this purpose have tended to ignore the effects of spatial population structure. However in many species, individual dispersal is restricted in space and fine-scale spatial structure such as isolation by distance (IBD) is commonly observed in continuous populations. Using a simulation-based approach, we investigated how comparative and single-point methods, traditionally used in a Wright-Fisher (WF) population context for detecting population size reduction, behave for IBD populations. We found that a complex 'quartet' of factors was acting that includes restricted dispersal, population size (i.e. habitat size), demographic history, and sampling scale. After habitat reduction, IBD populations were characterized by a stronger inertia in the loss of genetic diversity than WF populations. This inertia increases with the strength of IBD, and decreases when the sampling scale increases. Depending on the method used to detect a population size reduction, a local sampling can be more informative than a sample scaled to habitat size or vice versa. However, IBD structure led in numerous cases to incorrect inferences on population demographic history. The reanalysis of a real microsatellite data set of skink populations from fragmented and intact rainforest habitats confirmed most of our simulation results.

Alleles↗
PubMed2005

Association of interleukin-18 gene single-nucleotide polymorphisms with susceptibility to inflammatory bowel disease.

Interleukin-18 (IL-18) is believed to be one of the most important cytokines in the pathogenesis of inflammatory bowel disease (IBD). The aim of the study was to clarify the significance of single-nucleotide polymorphisms (SNPs) at the 5'-end of the IL-18 gene in the development of IBD. DNA was obtained from peripheral blood of 99 patients with ulcerative colitis (UC), 79 patients with Crohn's disease (CD), and 102 healthy controls. All participants were Japanese. SNPs at -656G/T, -607C/A, -137G/C, +113T/G, and +127C/T were determined by means of direct sequencing, and a genetic association with IBD was examined. The frequencies of the G allele at +113 and the T allele at +127 were significantly higher in patients with CD and UC compared with controls. The differences in allelic frequencies were more striking in patients with CD than in patients with UC, and at position +127 than at position +113. The haplotype estimation, according to the E-M algorithm, suggested that TACGT is closely associated with IBD, especially with CD. It was concluded that SNPs at the 5'-end of IL-18 gene might be closely related to the etiology of IBD.

Genetic Predisposition to Disease↗
PubMed2006

Association analysis of MYO9B gene polymorphisms and inflammatory bowel disease in a Norwegian cohort.

Association between single nucleotide polymorphisms (SNPs) within the MYO9B gene and celiac disease was recently reported. The role of MYO9B in celiac disease was suggested to relate to an epithelial barrier defect. The region to which MYO9B localize is also linked with inflammatory bowel disease (IBD). For these reasons, we hypothesize that MYO9B could also be a susceptibility gene in IBD. To address this, we performed an association study of a Norwegian IBD cohort (149 patients with Crohn's disease, 308 patients with ulcerative colitis and 562 healthy controls) using SNPs, which tagged the celiac disease associated MYO9B haplotype. No association between these SNPs and IBD was observed. Our results failed to support the notion that MYO9B is a susceptibility gene in IBD.

Colitis, Ulcerative↗
PubMed1992

Inflammatory bowel disease presenting in pregnancy.

A case of inflammatory bowel disease (IBD) presenting in pregnancy is described. Despite previous reports of severe fulminating disease in this type of patient, this woman did well with an uncomplicated course; she responded to standard medical therapy and there were no fetal complications. IBD should not be a contraindication to pregnancy unless the disease is poorly controlled. Pregnancy does not increase the risk of relapse of IBD, but should this occur it is more likely in the first trimester or in the postpartum period. Treatment of IBD in pregnancy should be much the same as in the nonpregnant woman. Corticosteroids and sulphasalazine are safe in pregnancy and are the mainstays of medical treatment. Surgery should proceed for the usual indications of toxic megacolon and perforation. In the group requiring surgery fetal mortality is considerable but the maternal outcome is improving. Patients presenting with IBD in pregnancy may have more severe disease but recent reports suggest that the outcome for mother and infant in this group is improving.

Adult↗