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PubMed1997

Clinical uniformity of inflammatory bowel disease a presentation and during the first year of disease in the north and south of Europe. EC-IBD Study Group.

OBJECTIVE: To compare the methods used for diagnosis and the clinical features of non-specific inflammatory bowel disease (IBD) in the north and south of Europe. DESIGN: A prospective study over 2 years in 1991-3 at eight centres in the north and 12 in the south of Europe using the same criteria for disease definition and same protocol for recording data. SETTING: Specialist gastroenterological centres with good diagnostic facilities at which every effort was made to ascertain all new cases of IBD seen in other departments and primary care in a defined geographical area of known population. PARTICIPANTS: A total of 2201 patients newly diagnosed as suffering from IBD, 1397 with ulcerative colitis (UC), 706 with Crohn's disease (CD) and 116 with indeterminate colitis (IND). RESULTS: Diagnostic methods used were similar in north and south, a biopsy or resection specimen was available for examination in 94 and 95%, of cases of UC and 92 and 87% of CD in north and south, respectively. The type, clinical presentation, site and extent of disease were similar in north and south. Treatment followed a common pattern and mortality from IBD was low in the first year after diagnosis. In both areas, age of onset of UC tended to be later than CD. CONCLUSION: The standard of diagnosis and clinical features of IBD are similar in specialist centres throughout Europe so providing a valid basis for this aspect of collaborative epidemiological or other studies.

Adult↗
PubMed2004

Regulation of gene expression in inflammatory bowel disease and correlation with IBD drugs: screening by DNA microarrays.

Potential biomarkers for Crohn's disease (CD) and ulcerative colitis (UC) were identified from two sets of full thickness pathologic samples utilizing DermArray and PharmArray DNA microarrays relative to uninvolved (Un) colon or normal colon. Seven of the over-expressed genes were verified using quantitative RT-PCR (i.e., TMPT, FABP1, IFI27, LCN2, COL11A2, HXB, and metallothionein). By correlating gene expression profiles between inflammatory bowel disease (IBD) tissue samples and IBD drug-treated cell cultures it might be possible to identify new candidate molecular target genes for IBD therapy and drug discovery. Potential biomarkers for CaCo2 cell cultures, which are routinely used as a GI tract surrogate model for in vitro pharmacokinetic studies, treated with azathioprine, 5-aminosalicylic acid, metronidazole, and prednisone were also identified from another experiment. Metallothionein mRNA expression was found to be down-regulated in azathioprine-treated CaCo2 cells, and was coincidentally up-regulated in the CD sample, thus resulting in an anti-correlation. These results suggest that this new screening methodology is feasible, that metallothioneins might be biomarkers for azathioprine therapy in vivo in CD, and that azathioprine might mechanistically down-regulate metallothionein gene expression. Correlations were also observed between IBD samples and either metronidazole- or 5-aminosalicylic acid-treated CaCo2 cells. Similar comparisons of disease tissue samples in vivo vs drug-treated cell cultures in vitro might reveal new mechanistic insights concerning established or experimental drug therapies. This affordable in vitro methodology is promising for expanded studies of IBD and other diseases.

Adult↗
PubMed2006

Indeterminate colitis: a significant subgroup of pediatric IBD.

BACKGROUND: Indeterminate colitis (IC) is a subgroup of inflammatory bowel disease (IBD) that cannot be characterized as either ulcerative colitis (UC) or Crohn's disease (CD). Our aims are to determine the prevalence of IC in our pediatric patient population and to describe its clinical presentation, natural history,and disease distribution. METHODS: We performed a retrospective database analysis of all children diagnosed with IBD at the Johns Hopkins Children's IBD Center between 1996 and 2001. Patient demographics, including age, sex, and age at disease onset, were tallied. Disease distribution was identified on the basis of a review of all endoscopic, colonoscopic, histopathological, and radiological records. All of the patients were followed up clinically to determine the extent of disease progression on the basis of the initial diagnosis of IC. RESULTS: Among 250 children registered in the database, 127 (50.8%) had a diagnosis of CD, 49 (19.6%) had UC, and 74(29.6%) had IC. Patients with IC had a significantly younger mean +/- SEM age (9.53 +/- 4.8 years) at diagnosis compared with patients with CD (12.4 +/- 3.8 years; P < 0.001) but not compared with patients with UC (7.41 +/- 3.5 years). Among the patients with IC, 59 (79.7%) had a pancolitis at diagnosis, and the remaining 15 had left-sided disease that progressed to a pancolitis within a mean of 6 years. Twenty-five patients (33.7%) with an initial diagnosis of IC were reclassified to either CD or UC after a median follow-up of 1.9 years (range 0.6-4.5 years). Forty-nine patients (66.2%) maintained their diagnosis of IC after a mean follow-up of 7 years (SEM 2.5 years). CONCLUSIONS: IC is a distinct pediatric subgroup of IBD with a prevalence that is higher than that observed in adults. Children with IC have an early age of disease onset and a disease that rapidly progresses to pancolitis. Longitudinal studies are needed to determine the clinical implications of this pediatric IBD subgroup.

Adolescent↗
PubMed2003

Thioguanine: a potential alternate thiopurine for IBD patients allergic to 6-mercaptopurine or azathioprine.

OBJECTIVE: Approximately 10% of inflammatory bowel disease (IBD) patients receiving 6-mercaptopurine (6-MP) or azathioprine (AZA) develop drug hypersensitivity reactions necessitating early discontinuation of these traditional thiopurines. These allergic reactions typically reoccur upon rechallenge. Our recently published pilot study suggested that thioguanine (6-TG), a closely related thiopurine, was efficacious and well tolerated in IBD patients resistant to 6-MP/AZA. The aim of this study was to determine if hypersensitivity reactions to 6-MP/AZA reoccur with 6-TG therapy. METHODS: IBD patients allergic to 6-MP and/or AZA were treated with 6-TG as an alternate thiopurine. Hypersensitivity reactions to 6-MP/AZA must have been documented within 6 wk of 6-MP/AZA initiation. RESULTS: 6-TG was initiated in 21 IBD patients at a median (range) dose of 20 (10-40) mg/day. 6-TG hypersensitivity reaction occurred in only four of 21 (19%) patients after a median time interval of 9 days. Pancreatitis did not reoccur with 6-TG. Eighty-two percent of 6-TG tolerant patients were assessed as improved at last follow-up. CONCLUSIONS: These results suggest that 6-TG may be considered as a possible alternate thiopurine in patients allergic to traditional 6-MP/AZA. Despite these favorable results, candidates for 6-TG should be selected with caution, and its use should be reserved for IBD patients well informed about potential toxicities.

Adult↗
PubMed2006

Laboratory markers in IBD: useful, magic, or unnecessary toys?

Laboratory markers have been investigated in inflammatory bowel disease (IBD) for diagnostic and differential diagnostic purposes, for assessment of disease activity and risk of complications, for prediction of relapse, and for monitoring the effect of therapy. The introduction of biological therapies in IBD has renewed interest in inflammatory markers (especially C reactive protein (CRP)), given their potential to select responders to these treatments. Of all the laboratory markers, CRP is the most studied and has been shown to have the best overall performance. CRP is an objective marker of inflammation and correlates well with disease activity in Crohn's disease (CD). Increased CRP levels are associated with better response rates and normal CRP levels predict high placebo response rates in clinical trials with biologicals. However, despite the advantages of CRP over other markers, it is still far from ideal. Furthermore, CRP correlates less well with disease activity in patients with ulcerative colitis (UC) as compared with CD. Other laboratory markers, including erythrocyte sedimentation rate (ESR), leucocyte and platelet count, albumin, and 1 acid glycoprotein (orosomucoid), have been studied either less extensively in IBD or have proven to be less useful than CRP. Faecal markers seem promising and may be more specific in detecting gut inflammation in patients with established IBD. Promising results have been reported with the use of faecal calprotectin in CD as well as in UC. Recent data however suggest that the performance of the faecal calprotectin test is superior for UC than for CD. Taken together, laboratory markers are useful and should be part of the global management of our IBD patients. They are however not magic and until more data become available, the use of CRP and other laboratory markers should be seen as an additive tool to clinical observation and physical examination rather than a replacement.

Acute-Phase Reaction↗
PubMed2002

Statistics on continuous IBD data: exact distribution evaluation for a pair of full(half)-sibs and a pair of a (great-) grandchild with a (great-) grandparent.

BACKGROUND: Pairs of related individuals are widely used in linkage analysis. Most of the tests for linkage analysis are based on statistics associated with identity by descent (IBD) data. The current biotechnology provides data on very densely packed loci, and therefore, it may provide almost continuous IBD data for pairs of closely related individuals. Therefore, the distribution theory for statistics on continuous IBD data is of interest. In particular, distributional results which allow the evaluation of p-values for relevant tests are of importance. RESULTS: A technology is provided for numerical evaluation, with any given accuracy, of the cumulative probabilities of some statistics on continuous genome data for pairs of closely related individuals. In the case of a pair of full-sibs, the following statistics are considered: (i) the proportion of genome with 2 (at least 1) haplotypes shared identical-by-descent (IBD) on a chromosomal segment, (ii) the number of distinct pieces (subsegments) of a chromosomal segment, on each of which exactly 2 (at least 1) haplotypes are shared IBD. The natural counterparts of these statistics for the other relationships are also considered. Relevant Maple codes are provided for a rapid evaluation of the cumulative probabilities of such statistics. The genomic continuum model, with Haldane's model for the crossover process, is assumed. CONCLUSIONS: A technology, together with relevant software codes for its automated implementation, are provided for exact evaluation of the distributions of relevant statistics associated with continuous genome data on closely related individuals.

Chromosome Mapping↗
PubMed2006

Aggravation of intestinal inflammation by depletion/deficiency of gammadelta T cells in different types of IBD animal models.

The role of gammadelta T cells in inflammatory bowel disease (IBD) is still controversial. Although gammadelta T cells induce IBD in immunodeficient animals, others suggest a protective role of gammadelta T cells. Therefore, this study was conducted in order to elucidate the effect of gammadelta T cell depletion/deficiency on different IBD animal models. Mice depleted of or deficient in gammadelta T cells were exposed to dextran sodium sulfate (DSS) in order to induce colitis. In addition, gammadelta T cells were depleted in mice with terminal ileitis (TNFDeltaARE) or colitis due to interleukin 2 deficiency (IL-2 ko). Finally, DSS-induced colitis was studied in mice deficient in interferon gamma (IFN-gamma ko) upon gammadelta T cell depletion. Depletion of gammadelta T cells aggravated DSS-induced colitis and terminal ileitis of TNFDeltaARE mice. Exacerbated DSS-induced colitis was also found in gammadelta T cell-deficient mice. IL-2 ko mice showed increased mortality upon early (starting at 4 wk of age) but not late depletion (starting at 8 wk of age). Early gammadelta T cell depletion or deficiency resulted in increased IFN-gamma production by both lamina propria lymphocytes and splenocytes in every model investigated herein. In IFN-gamma ko mice, gammadelta T cell depletion did not affect the development and course of DSS-induced colitis. The protective effect of gammadelta T cells in IBD was confirmed in various IBD animal models. Particularly, during the early phase of intestinal inflammation, gammadelta T cells appear to be important. The mechanism seems to involve the control of IFN-gamma production and epithelial regeneration.

Animals↗
PubMed1998

Soluble mediators and the interaction of drugs in IBD.

The chronic idiopathic bowel diseases (IBD) - Crohn's disease and ulcerative colitis - are considered to be the result of an unrestrained inflammatory reaction. Although an explanation for the etiopathogenesis has still not emerged, the explosion of information on the inflammatory process is expected to yield a multitude of drugs targeted at particular elements of the inflammatory process. The final common pathway of immune activation in IBD is the local influx of monocytes, macrophages and polymorphonuclear neutrophils (PMNs). The processes which account for the recruitment of these cells include cytokine generation, complement activation and eicosanoid biosynthesis. Once the influx of PMNs and macrophages occurs, an increased production of platelet-activating factor (PAF) and leukotrienes (LTs), in particular LTB(4), results in the secondary amplification of the inflammatory response, which provides the clinical manifestations of IBD. Other important soluble mediators of inflammation include complement-derived and chemotactic peptides, specific adhesion molecules, neuropeptides and reactive metabolites of oxygen and nitrogen. Current established therapies, such as glucocorticoids and 5-aminosalicylic acid (5-ASA), inhibit raised concentrations of these interdependent soluble mediators of inflammation, which may amplify one another or have parallel effects. Future medical options for treatment of IBD aim at removing perpetuating antigens or inhibiting the entry of inflammatory cells by manipulating adhesion molecules, by blocking the proinflammatory molecules, or by preserving endogenous suppressive molecules or correcting genetic defects. However, it remains to be defined whether targeting multiinflammatory actions or a single key pivotal process is the better therapeutic strategy and whether subgroups of IBD with different clinical courses will require different treatment approaches.

Journal Article↗
PubMed2002

Estimation of Sjögren's syndrome among IBD patients. A six year post-diagnostic prevalence study.

OBJECTIVE: To study the prevalence of Sjögren's syndrome (SS), tear and saliva production and sicca symptoms in patients with inflammatory bowel disease (IBD) seen six years after IBD diagnosis. METHODS: In a population based cohort of 654 patients with IBD, 521 patients (80%) and a control group consisting of 68 healthy subjects were investigated. SS was diagnosed according to the European Criteria proposed by the American-European Consensus Group (US-EU criteria) and the European criteria. Maximum (supposing positive biopsies) and minimum prevalences (supposing negative biopsies) were estimated. RESULTS: Dryness of eyes and mouth were similarly distributed between patients with ulcerative colitis (UC) and Crohn's disease (CD) and between patients and controls. The prevalence of SS was 0-4.2% and 0-5.7% (minimum-maximum) according to the US-EU criteria and the European criteria, respectively. The controls fulfilled neither of the criteria. CONCLUSION: Sjögren's syndrome, sicca symptoms, tear and saliva production were not increased in patients with IBD compared to controls, indicating a lack of association between SS and IBD.

Adult↗
PubMed2003

Clinical applications of advances in the genetics of IBD.

Our rapidly expanding understanding of the genetics of inflammatory bowel disease (IBD) has led to important clinical applications. It is becoming apparent that genes help determine the clinical phenotype, intestinal and extraintestinal complications, response to treatment, and drug toxicities in these disorders. For example, NOD2/CARD15 mutations are associated with ileal Crohn's disease, possibly with a fibrosing/obstructing phenotype, but do not influence responses to infliximab treatment. Similarly, certain human leukocyte antigen (HLA) haplotypes are associated with aggressive, extensive ulcerative colitis and strongly influence extraintestinal manifestations of IBD, including uveitis and various forms of arthritis. Expression of the glucocorticoid receptor b determines the clinical response to corticosteroids, whereas genetically regulated levels of enzymes metabolizing 6-mercaptopurine/azathioprine may determine clinical responses and toxicities to these important immunosuppressive agents. Once we have a more sophisticated understanding of the mechanisms of genetic defects in IBD, it may be feasible to restore physiologic function to prevent the onset of disease in susceptible individuals. However, because we do not have the ability to prevent disease at the present time, it is premature to screen offspring and first-degree relatives of IBD patients for the NOD2/CARD15 genotype. One can anticipate that it will become feasible to prospectively determine a patient's genotype and to individualize a drug regimen, leading to highly effective, safe treatments for IBD patients on a rational, rather than empiric, basis.

Carrier Proteins↗
PubMed2003

[Extra-intestinal manifestation of IBD in Veszprém county (of Hungary): results of a 25-years follow-up study].

INTRODUCTION: IBD is a systemic disease associated with a number of extraintestinal manifestations (EIM). The author's aim was to determine the prevalence and features of EIM in a large IBD population in Veszprém county in a 25-year follow-up study. PATIENTS AND METHODS: 873 IBD patients were enrolled in the study (UC: 619, m/f: 317/302, age at presentation: 38.3 yrs, disease duration: 11.2 yrs; CD: 254, m/f: 125/129, age at presentation: 32.5 yrs, disease duration: 9.2 yrs). Intestinal, extraintestinal symptoms and laboratory tests were monitored regularly. Any alteration suggesting an EIM was investigated by specialist. RESULTS: A total of 21.3% of patients with IBD patients had EIM (UC: 15.0%, CD: 36.6%). Age at presentation did not affect the likelihood of EIM. Prevalence of EIM was higher in women and in CD, ocular complications and PSC were more frequent in UC. In UC there was an increased tendency of EIM in patients having a more extensive disease. In CD patients colonic location increased the frequency of axial and type-1 peripheral arthritis. In UC positive family history increased the risk of joint (OR: 3.63) complications. Joint complications were more frequent in CD (22.4%) than in UC (10.2%, p < 0.01). PSC was present in 1.6% in UC and 0.8% in CD. Dermatological complications were present in 3.8% in UC and 10.2% in CD, the rate of ocular complications was around 3% in both diseases. Erythema nodosum, pyoderma gangrenosum and uveitis were the most frequent manifestations among them. Rare complications were glomerulonephritis, autoimmune haemolytic anaemia and celiac disease. CONCLUSION: The prevalence of EIM in Hungarian IBD patients was in concordance with data from Western countries. The high number of EIM supports a role for complex follow-up in these patients.

Adolescent↗
PubMed2005

The IBD international genetics consortium provides further evidence for linkage to IBD4 and shows gene-environment interaction.

BACKGROUND AND AIMS: The inflammatory bowel diseases (IBDs) Crohn's disease (CD) and ulcerative colitis are complex disorders with an important genetic determinant. One gene associated with CD has been identified: NOD2/CARD15. Two independent genome-wide scans found significant evidence (logarithm of odds [LOD] 3.6) and suggestive evidence (LOD 2.8) for linkage on locus 14q11-12, also known as the IBD4 locus. To further characterize this locus, we assessed gene-environment interaction (IBD4 x smoking) and phenotypic heterogeneity in a large cohort of IBD-affected sibling pairs as part of an ongoing international collaborative effort. PATIENTS AND METHODS: A total of 733 IBD families, comprising 892 affected sibling pairs, were genotyped for microsatellites D14S261, D14S283, D14S972, and D14S275, spanning the IBD4 locus. Information on gender, ethnicity, age at onset, smoking at diagnosis, extraintestinal manifestations, and disease location was available. RESULTS: A significant distortion in the mean allele sharing (MAS) between affected siblings was observed for CD patients only at each of the four markers (54.6%, 52.8%, 50.4%, and 53.3%, respectively). Maximum linkage for CD was observed at marker D14S261 (multipoint nonparametric linkage score 2.36; P </= 0.01; MAS 54.6%). MAS was higher in CD families in which all siblings or at least one sibling smoked compared with nonsmoking CD families (MAS, 58.90%, 57.50%, and 52.80%, respectively). CONCLUSIONS: The IBD International Genetics Consortium replicated the IBD4 locus on chromosome 14q for CD and also showed evidence for a gene-environment interaction at this locus. Further studies are needed to explore the mechanism by which smoking influences IBD4.

Adolescent↗
PubMed2001

Quality of health care in inflammatory bowel disease: development of a reliable questionnaire (QUOTE-IBD) and first results.

OBJECTIVES: As inflammatory bowel disease is a chronic disorder, usually with an early onset in life, quality of care plays an important role for patients. The aim of this study was to develop a questionnaire to measure quality of care through the eyes of patients with inflammatory bowel disease. METHODS: Ten generic questions were already available because the questionnaire is based on an existing instrument. Patients with inflammatory bowel disease in seven countries were involved in the development of additional disease-specific items. Validation and first field testing of the total questionnaire (QUOTE-IBD) was performed in The Netherlands. RESULTS: A total of 380 patients cooperated in the development of 13 disease-specific items, with high internal reliability (Cronbach's alpha = 0.83). Another 162 patients were involved in validating and testing of the QUOTE-IBD, which consists of 23 items in total. Pearson's correlation coefficient between QUOTE-IBD and visual analog scale scores of health care items was 0.55. Intraclass correlation coefficient of two assessments was 0.64. First testing showed that patients gave relatively poor marks to some part of health care services, such as providing information about extraintestinal complaints and the psychological as well as physical approach to complaints. CONCLUSIONS: A short, valid, reliable questionnaire was developed to measure the opinions of patients with inflammatory bowel disease on quality of health care. The QUOTE-IBD can be used for identification of areas for improvement, with the aim of optimizing health care in inflammatory bowel disease.

Europe↗
PubMed1995

A chromosome-based method to infer IBD scores for missing and ambiguous markers.

We propose a probability model to impute missing identical-by-descent (IBD) vectors for linkage analysis, when adjacent marker loci are typed and interference is estimable. A chromosome-based IBD distribution, conditioned on available marker data, is computed using a fast algorithm to estimate the joint probability of genes IBD at several equally spaced linked loci. Weighted IBD vectors are then used in various test statistics for linkage analysis. As an example, we analyzed the 18 affected sib pairs in the GAW9 Problem 1 data set using Risch's lod-score test.

Algorithms↗
PubMed2007

The prevalence of genetic and serologic markers in an unselected European population-based cohort of IBD patients.

BACKGROUND AND AIM: The aetiology of inflammatory bowel disease (IBD) is unknown, but it has become evident that genetic factors are involved in disease susceptibility. Studies have suggested a north-south gradient in the incidence of IBD, raising the question whether this difference is caused by genetic heterogeneity. We aimed to investigate the prevalence of polymorphisms in CARD15 and TLR4 and occurrence of anti-Saccharomyces cerevisiae (ASCA) and antineutrophil cytoplasmic antibodies (pANCA) in a European population-based IBD cohort. METHODS: Individuals from the incident cohort were genotyped for three mutations in CARD15 and the Asp299gly mutation in TLR4. Levels of ASCA and pANCA were assessed. Disease location and behaviour at time of diagnosis was obtained from patient files. RESULTS: Overall CARD15 mutation rate was 23.9% for CD and 9.6% for UC patients (P < 0.001). Mutations were less present in the Scandinavian countries (12.1%) versus the rest of Europe (32.8%) (P < 0.001). Overall population attributable risk was 11.2%. TLR4 mutation rate was 7.6% in CD, 6.7% in UC patients and 12.3% in healthy controls (HC), highest among South European CD patients and HC. ASCA was seen in 28.5% of CD patients with no north-south difference, and was associated with complicated disease. pANCA was most common in North European UC patients and not associated with disease phenotype. CONCLUSION: The prevalence of mutations in CARD15 varied across Europe, and was not correlated to the incidence of CD. There was no association between mutations in TLR4 and IBD. The prevalence of ASCA was relatively low; however related to severe CD.

Antibodies, Antineutrophil Cytoplasmic↗
PubMedDate not supplied

Coping patterns and related characteristics in patients with IBD.

This article describes a study designed to examine the coping behaviors, personality, and mood characteristics of 150 nonhospitalized adults with inflammatory bowel disease (IBD). Self-report questionnaires and interviews were used to collect the data. Coping responses were measured with the Jalowiec Coping Scale. The Eysenck Personality Questionnaire (EPQ) and Beck Depression Inventory (BDI) were used to ascertain other characteristics. Data were analyzed using analysis of variance (ANOVA), Pearson's correlation coefficient (r), and descriptive statistics. IBD patients scored significantly higher on using problem-oriented coping patterns than on using affective-oriented methods. The results suggest that coping patterns in IBD patients are remarkably effective in contributing to lifestyle satisfaction. It can be inferred that adaptive efforts of IBD patients can be enhanced if health professionals consider coping patterns in the assessment process and if they actively support a sense of control in these patients.

Activities of Daily Living↗
PubMed1990

IgG subclass-containing cells in the human large bowel of normal controls, non-IBD colitis, and ulcerative colitis.

IgG subclass-containing cells in colonic mucosa were examined in three groups; 1) normal controls 2) cases of ulcerative colitis (UC) 3) cases of colitis excluding UC and Crohn's disease (non-IBD colitis) by indirect immunoperoxidase staining method using mouse anti-IgG subclass monoclonal antibodies. The numbers (and proportions) of IgG1, IgG2, IgG3, and IgG4-containing cells in normal colonic mucosa was 80 +/- 29/mm2 (44.6%), 44 +/- 21 (24.1%), 44 +/- 24 (23.7%), 13 +/- 10 (7.7%), respectively. The proportion of IgG subclass-containing cells in normal colonic mucosa was different from the known proportion of IgG subclass in serum. In UC, the numbers of all IgG subclasses-containing cells were significantly increased compared to controls and non-IBD colitis. However, only IgG1-containing cells were increased in proportion (50.3%) compared to normal controls. In non-IBD colitis, the numbers of IgG1- and IgG2-containing cells were increased compared to the controls, but the increases were less than UC, and there was no difference in the proportion of IgG subclass compared to normal controls. The differences in the numbers and in the proportions of IgG subclass-containing cells between UC and non-IBD colitis may reflect differences in the underlying disease process.

Adolescent↗
PubMed2004

Activation of NF-kappaB in intestinal epithelial cells by E. coli strains isolated from the colonic mucosa of IBD patients.

BACKGROUND AND AIMS: The involvement of bacteria in the pathogenesis of inflammatory bowel disease has been discussed for several years. In this study we evaluated the ability of E. coli isolates from inflamed and noninflamed colonic mucosa to activate NF-kappaB. MATERIALS AND METHODS: Fifteen bacterial strains from inflamed and six from noninflamed colonic tissues from IBD patients. Their ability to induce NF-kappaB activation was examined in vitro by gel-shift assays. The activation of the TNF-alpha promoter was determined by reporter gene assays. Bacterial isolates were characterized by invasion assays, electron microscopy, and PCR. RESULTS: Four of 15 E. coli bacterial isolates from inflamed IBD tissues induced NF-kappaB activity in intestinal epithelial cells as determined by gel-shift assays. NF-kappaB activation was only seen with living bacteria but not with heat-inactivated cells. Isolates from noninflamed tissues and a wild-type E. coli control strain induced a weaker or no activation. Reporter gene assays with a construct comprising a luciferase gene driven by the TNF-alpha promoter revealed that isolates from Crohn's disease patients induced a stronger activation of the TNF-alpha gene than isolates from ulcerative colitis patients. The isolated bacteria invaded HT-29 cells, although typical virulence genes for enteropathogenic, enterhemorrhagic, or enteroinvasive E. coli, i.e., eae, tir, EspA, Per (A-C), ipaC, were not detected in these cells. Bacterial invasion was additionally confirmed by electron microscopy examination. CONCLUSION: Our results indicate that E. coli strains can be found in the mucosa of some IBD patients which are able to activate NF-kappaB similar to known pathogenic strains. The absence of several virulence genes in these cells suggests that they are members of the luminal flora which acquire as yet unidentified virulence determinants and are therefore involved in the pathophysiology of IBD.

Colon↗