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PubMed1997

Circulating antioxidants in ulcerative colitis and their relationship to disease severity and activity.

Oxygen free radicals produced by neutrophils are important in the pathogenesis of mucosal damage in ulcerative colitis. Vitamin A, vitamin E and cysteine in the plasma can scavenge free radicals. In the present study, plasma levels of vitamin A, vitamin E, cysteine, cystine and protein-bound cysteine were measured in active ulcerative colitis before and immediately after treatment of the active disease, and correlated with disease severity, extent and activity. Plasma vitamin A and cysteine were significantly reduced in active ulcerative colitis compared with controls. Levels of vitamin E, cystine and protein-bound cysteine were not significantly altered in active ulcerative colitis. Vitamin A and cysteine concentrations returned to normal levels (P < 0.05) within 2 weeks of treating active colitis. There were significant negative correlations between clinical severity and the plasma concentrations of vitamin A and cysteine. Plasma cysteine levels also correlated inversely to disease extent. Depletion of the circulating antioxidants, vitamin A and cysteine, in active ulcerative colitis is likely to be important in the pathophysiology of the disease.

Adolescent↗
PubMed2004

Hyperexpression of inducible costimulator on lamina propria mononuclear cells in rat dextran sulfate sodium colitis.

BACKGROUND AND AIMS: The authors have previously shown that a third member of the CD28 family, inducible costimulator (ICOS), was increased in the inflamed intestinal mucosa of murine experimental colitis, and that the blockade of ICOS ameliorated the development of colitis. However, the role of ICOS in rat intestinal inflammation and its expression profile remains unclear. In the present study, the authors investigated the involvement of ICOS in the development of rat dextran sulfate sodium (DSS)-induced colitis, and the therapeutic potential of anti-ICOS monoclonal antibody (mAb) in colitis. METHODS: The authors first examined expression of ICOS protein in normal rat by immunohistochemistry and flow cytometry. Sprague-Dawley rats were fed 3.0% DSS. The expression of ICOS on infiltrating lamina propria mononuclear cells and splenocytes were examined. The DSS-fed rats were then administered anti-ICOS mAb to test its effect on the development of colitis. RESULTS: Unlike mice and human, ICOS was expressed on a part of CD4+ T-cells from the thymus, spleen, mesenteric lymph nodes and lamina propria. Levels of ICOS on CD4+ T-cells from the spleen and colonic lamina propria were significantly upregulated after Concanavalin A (Con A) stimulation. In addition, ICOS was also upregulated on CD4+ T-cells from DSS-fed rats compared with those from non DSS-fed rats. However, anti-ICOS mAb did not ameliorate the development of both acute and chronic DSS colitis. CONCLUSION: These results suggest that the different expression of ICOS in rats plays a distinct role in rat intestinal inflammation.

Animals↗
PubMed2004

Restorative proctocolectomy in patients with ulcerative colitis having a recto-vaginal fistula.

OBJECTIVE: Recto-vaginal fistula is a rare complication of ulcerative colitis. There are few reports of restorative proctocolectomy carried out in patients with ulcerative colitis having a rectovaginal fistula. We report our experience with this condition. PATIENTS AND METHODS: Between 1 January 1976 and 31 December 2001, 838 patients underwent restorative proctocolectomy for ulcerative colitis at one hospital. These included 400 women of whom 4 (1%) had an already present rectovaginal fistula. We reviewed all patients who presented with a rectovaginal fistula. These patients were contacted by telephone to establish function and satisfaction. RESULTS: The mean age was 30.0 years (range 19-39 years). The mean age at onset of ulcerative colitis was 21.5 years (range 13-34 years). One patient was asymptomatic, the fistula being discovered at operation. In the other three patients the recto-vaginal fistula had occurred at a mean of 108 months (range 72-192 months) after the onset of ulcerative colitis. Three of four patients had had previous episodes of acute severe disease. Three patients had a narrow rectum with deep ulceration. The mean distance between the anorectal junction and the site of fistulation was 2.7 cm (range 0-7 cm). Three patients had a three-stage and one patient a two-stage procedure. Mean follow-up after closure of the loop ileostomy was 107 months (range 17-276 months). All patients were treated successfully but 2 (50%) had a recurrence at 156 and 40 months after the closure of the loop ileostomy. One patient was diverted and the fistula was closed by a subsequent transanal repair and the other patient was treated with success by temporary loose seton technique. Two patients had excellent functional results whereas two other had some difficulties in continence. Nevertheless all patients were satisfied with the outcome. CONCLUSIONS: Patients with ulcerative colitis and a recto-vaginal fistula can be successfully treated by restorative proctocolectomy, nevertheless they are at risk of late recurrence of the fistula.

Adult↗
PubMed1999

Colitis may be part of the antiepileptic drug hypersensitivity syndrome.

PURPOSE: To show that colitis may be part of the antiepileptic hypersensitivity syndrome. METHODS: Description of two case histories. RESULTS: The first patient was a 47-year-old man who developed fever, lymphadenopathy, influenza-like symptoms, facial edema, skin rash and diarrhea after 3 weeks of carbamazepine (CBZ) treatment. Laparotomy because of severe abdominal pain 2 weeks later showed severe colitis with perforations. The second patient was a 41-year-old woman who developed fever, diarrhea, and skin rash 4 weeks after start of CBZ treatment. A colon biopsy confirmed colitis. Stool examinations did not show pathogenic microorganisms, and there was no evidence of Crohn's disease or ulcerative colitis. Both patients had elevated liver enzymes, peripheral eosinophilia, and eosinophils in the infiltrate of the colon. CONCLUSIONS: In view of the close temporal relation between start of CBZ intake and development of colitis, the presence of fever, lymphadenopathy, and rash, and improvement after discontinuation of CBZ, we conclude that the two patients developed an AED hypersensitivity syndrome. Our case histories demonstrate that severe colitis may be part of this syndrome.

Adult↗
PubMed1998

Microsatellite instability in non-neoplastic mucosa of patients with ulcerative colitis: effect of folate supplementation.

OBJECTIVE: Microsatellite instability (MSI) detected in non-neoplastic mucosa of patients with ulcerative colitis has been ascribed to an excess of DNA damage associated with chronic inflammation. Folate deficiency, commonly found in patients with long-standing disease, could further contribute to this defect because folate is essential for DNA replication and repair. We evaluated MSI in the colonic mucosa of 26 patients with ulcerative colitis for >10 yr and 10 patients with Crohn's colitis and correlated MSI with folate status. METHODS: DNA was amplified using primers directed at nine different loci. Folate concentrations in serum, whole blood, and colonic mucosa were determined using the Lactobacillus casei assay. RESULTS: MSI was found in 3/23 patients (13%) with ulcerative colitis and in none of the patients with Crohn's colitis. All three patients with MSI had inactive histological disease, whereas all patients with active disease were negative for MSI (p = 0.08). Serum, whole blood, and colonic concentrations of folate were 30-50% lower in patients with MSI (p > 0.05), and folate supplements had been administered less frequently during the past 5-yr (p = 0.06). One of the patients with MSI was randomized to receive folate 5 mg/d for 6 months, and a clear change in MSI pattern was observed in three of six markers. CONCLUSIONS: A defect in DNA repair associated with a low folate status may be one additional cause for patients with ulcerative colitis exhibiting MSI in non-neoplastic mucosa.

Colitis, Ulcerative↗
PubMed1998

Fecal hydrogen sulfide production in ulcerative colitis.

OBJECTIVE: Sulfide, a product of sulfate-reducing bacteria, has been proposed to play an etiologic role in ulcerative colitis. Ulcerative colitis feces have increased numbers and activity of sulfate-reducing bacteria, but only modestly increased sulfide. However, fecal sulfide exists largely in the volatile, highly toxic H2S form that moves rapidly from feces to surrounding gas. Our aim was to quantify the fecal release of H2S and other volatiles (CO2, H2, CH4, methanethiol, and dimethylsulfide). METHODS: Fecal samples from 25 subjects with ulcerative colitis and 17 controls were incubated in 4-L containers, and gas release was assessed at intervals over 24 h. RESULTS: H2S release by ulcerative colitis feces was elevated 3-4-fold at every measurement point compared with normal feces (p < 0.003 at 24 h). The only other significant difference was increased CO2 release by ulcerative colitis feces at 1 h. Supplementation of fecal homogenates with sulfur-containing substrates showed that organic compounds (mucin, cysteine, taurocholate) provided more readily utilizable substrate for H2S production than did sulfate. CONCLUSIONS: Increased H2S release is a relatively localized metabolic aberration of ulcerative colitis feces. This increased H2S may reflect abnormalities of the fecal bacteria and/or substrate availability.

Adolescent↗
PubMed2000

Right colonic involvement is associated with severe forms of ischemic colitis and occurs frequently in patients with chronic renal failure requiring hemodialysis.

OBJECTIVE: The aim of this study was to identify factors associated with severe outcome in patients with ischemic colitis. METHODS: The files of 60 consecutive inpatients (34 women, 26 men, mean age 67 yr) with ischemic colitis were reviewed. The following data were analyzed: age, sex, smoking, medications, history of cardiovascular disease, metabolic disease, chronic renal failure and hemodialysis, the time elapsed between the first symptoms and the diagnosis, and the site and extension of their colonic involvement. Patients were divided into two groups according to outcome: those with severe disease, including those who died from ischemic colitis (n = 3) or who required surgical resection (n = 21); and those with mild forms of colitis who were treated successfully without surgery (n = 36). The two groups were compared by means of univariate and multivariate analysis to identify factors associated with unfavorable outcomes. Only patients who had a complete examination of the colon (n = 51) were entered into the statistical analysis. RESULTS: By univariate analysis, chronic renal failure (p = 0.03), hemodialysis (p = 0.01), short delay between symptoms and diagnosis (p = 0.01), and right colonic involvement (p = 0.002) were significantly more common in the patients with severe colitis. By logistic regression, right colonic involvement was the only factor independently associated with severity (p = 0.01). Right-sided lesions were present in 82% of patients on dialysis but in only 26% of patients not on dialysis (p = 0.0005). CONCLUSIONS: Right colonic involvement is associated with severe forms of ischemic colitis and occurs frequently in patients with chronic renal failure requiring hemodialysis.

Adult↗
PubMed2000

High prevalence of celiac sprue-like HLA-DQ genes and enteropathy in patients with the microscopic colitis syndrome.

OBJECTIVE: Celiac sprue is associated with specific HLA-DQ genes (mainly DQ2). Because there are epidemiological and histopathological similarities between celiac sprue and microscopic colitis, we hypothesized that these syndrome may share an HLA genetic predisposition and pathogenesis. METHODS: The HLA-DQ genes of 25 patients with celiac sprue, 53 patients with the microscopic colitis syndrome, and 429 normal controls were typed and compared. Serum was analyzed for antigliadin and antiendomysial antibodies. Small intestinal biopsies were analyzed for signs of histopathology. RESULTS: HLA-DQ2 or DQ1,3 (the latter as DQ1,7,DQ1,8, or DQ1,9) were seen more frequently in both patient groups relative to controls. In patients with the microscopic colitis syndrome, serological tests for celiac sprue were weakly positive in 17%; mild inflammation of the small intestine without villous atrophy was present in 43%, and inflammation plus partial or subtotal villous atrophy was present in 27%. CONCLUSIONS: A shared set of predisposing HLA-DQ genes account for the epidemiological overlap of celiac sprue and microscopic colitis. Mild to moderate mononuclear cell inflammation of the small intestine, often accompanied by partial or subtotal villous atrophy, is frequent in patients with the microscopic colitis syndrome. Although further studies will be necessary to determine if this enteropathy is induced by dietary gluten, we speculate that the small intestinal but not colonic histopathology in patients with microscopic colitis is caused by immunological gluten sensitivity.

Adult↗
PubMed2000

Intravenous azathioprine in severe ulcerative colitis: a pilot study.

OBJECTIVE: Azathioprine use in acute ulcerative colitis has been limited by its perceived long onset of action. The aim of this study was to determine the safety and clinical effect of an i.v. loading dose of azathioprine in the setting of severe steroid refractory ulcerative colitis. METHODS: Nine hospitalized patients with severe steroid refractory ulcerative colitis were enrolled. Patients 1-3 received 20 mg/kg i.v. azathioprine over 36 h. Patients 4-6 received 40 mg/kg i.v. azathioprine over 36 h. Patients 7-9 received 40 mg/kg i.v. azathioprine as three 8-h infusions over 3 days. Clinical remission was defined as steroid withdrawal and an Ulcerative Colitis Disease Activity Index score of 0. The Inflammatory Bowel Disease Questionnaire was obtained at each visit. White blood cell concentrations and erythrocyte concentrations of 6-thioguanine were obtained. RESULTS: Five of nine patients (56%) had a response and avoided colectomy. Three of nine patients (33%) met the definition for clinical remission. Response was seen within 4 wk. The mean 6-thioguanine concentration for those five patients at 12 wk after infusion was 148.2 pmol/8 x 10(8). Two patients had transient leukopenia and one had transient hepatotoxicity. CONCLUSIONS: Intravenous azathioprine appears to be safe and of clinical benefit in inducing response and avoiding colectomy in severe steroid refractory ulcerative colitis. Data from an i.v. azathioprine trial in Crohn's disease suggests oral dosing alone may obtain the same results. The role of oral dosing alone in severe ulcerative colitis and the role of azathioprine metabolite levels in monitoring efficacy should be investigated further.

Adult↗
PubMed2001

Medical diagnoses and procedures associated with clostridium difficile colitis.

OBJECTIVES: The aim of this study was to examine the associations of Clostridium difficile colitis with other comorbid conditions and procedural interventions among hospitalized patients. METHODS: The Patient Treatment File of the Department of Veterans Affairs contains the computerized records of all inpatients treated in 172 Veterans Affairs hospitals distributed throughout the United States. The computerized medical records of 15,091 cases with C. difficile colitis and 61,931 controls without the diagnosis were extracted from the annual files between 1993 and 1998. In a multivariable logistic regression, the occurrence of C. difficile colitis served as outcome variable, whereas the occurrences of other diagnoses or procedures served as predictor variables. RESULTS: The total numbers of diagnoses in the case and control group were 136,840 and 465,972, respectively. The numbers of procedures were 75,479 and 129,612, respectively. C. difficile colitis was significantly associated with HIV infection, candidiasis, malignant neoplasm and chemotherapy, malnutrition, pneumonia, aspiration pneumonitis, intestinal obstruction, diverticulitis, renal failure, urinary tract infection, decubitus, and osteomyelitis. Interventional procedures involving the respiratory tract, bone marrow biopsy, arterial and venous catheterization, urinary catheterization, dialysis, gastrostomy tube, and physical therapy were also frequently associated with the development of C. difficile colitis. CONCLUSIONS: These associations reflect the influence of causal relationships (such as the use of antibiotics and chemotherapy), an increased risk of exposure to C. difficile among immobilized bedridden patients with chronic disease states, or a general system failure in patients with end-stage disease. Knowledge of such associations could help to alert physicians to an increased risk of C. difficile colitis among particular groups of susceptible patients.

Aged↗
PubMed2001

The comorbid occurrence of other diagnoses in patients with ulcerative colitis and Crohn's disease.

OBJECTIVES: The comorbidity between inflammatory bowel disease (IBD) and other diagnoses may help to shed light on the etiology and pathophysiology of IBD. The US Vital Statistics offer the opportunity to study causes of death broken down by comorbid disease associations. The aim of this study was to analyze the presence of comorbid conditions in persons who died from ulcerative colitis or Crohn's disease. METHODS: The numbers of deaths from ulcerative colitis and Crohn's disease were retrieved from the computerized 1991-1996 data files of the National Center for Health Statistics. Comorbid associations between other diagnosis and ulcerative colitis or Crohn's disease were expressed as age-, gender-, and race-standardized proportional mortality ratios. RESULTS: Ulcerative colitis and Crohn's disease showed, in general, similar patterns of comorbidity. Both diseases were associated with similar sets of GI complications, such as intestinal obstruction and stasis, mucosal inflammation and infection, vascular complications, and complications related to fistula and abscess formation. Extraintestinal complications of both IBD involved disorders of the hepatobiliary system, urinary system, and various coagulopathies. Ulcerative colitis alone was found to be associated with Hirschsprung's disease and schizophrenia, whereas Crohn's disease alone was found to be related with osteoporosis and amyloidosis. CONCLUSIONS: No completely unexplained or hitherto undescribed association was revealed. The numerous intestinal and extraintestinal complications associated with IBD serve as a reminder of the systemic nature and the resultant clinical severity of both ulcerative colitis and Crohn's disease.

Aged↗
PubMed2003

Risk of congenital abnormalities in children born to women with ulcerative colitis: a population-based, case-control study.

OBJECTIVES: It has recently been suggested that maternal ulcerative colitis is associated with an almost 4-fold increased risk of congenital abnormalities in offspring. We therefore examined the risk of congenital abnormalities in children born to women with ulcerative colitis. METHODS: This was a case-control study within the Hungarian Case Control Surveillance of Congenital Abnormalities, 1980-1996, based on 22,843 newborn children or fetuses with congenital abnormalities and 38,151 children without any detected congenital abnormalities (the control group). RESULTS: Seventy-one pregnant women (0.3%) had ulcerative colitis in the case group and 95 (0.2%) in the control group. The adjusted overall risk for having a child with congenital abnormalities in women with ulcerative colitis was OR = 1.3 (95% CI = 0.9-1.8). The risk of limb deficiencies, obstructive urinary congenital abnormalities, and multiple congenital abnormalities was OR = 6.2 (95% CI = 2.9-13.1), OR = 3.3 (95% CI = 1.1-9.5), and OR = 2.6 (95% CI = 1.3-5.4), respectively. No association was found for cleft lip with or without cleft palate or cardiovascular defects. CONCLUSIONS: We found no significantly increased overall risk of congenital abnormalities in children born to women with ulcerative colitis. However, our results indicate an increased risk of some selected congenital abnormalities (limb deficiencies, obstructive urinary congenital abnormalities, and multiple congenital abnormalities). More data are needed to determine whether the association between maternal ulcerative colitis and an increased risk of certain congenital abnormalities is causal or is influenced by bias.

Abnormalities, Multiple↗
PubMed2005

Is endoscopy necessary for the measurement of disease activity in ulcerative colitis?

OBJECTIVES: Many disease activity indices are used to measure ulcerative colitis. Invasive indices incorporate an endoscopic score, while noninvasive indices do not require endoscopy. In clinical practice, many patients are treated based on their symptoms without endoscopic evaluation. However, invasive indices are commonly used in clinical research. Our objective was to determine whether endoscopy is necessary for the assessment of disease activity in patients with ulcerative colitis. METHODS: Sixty-six consecutive ulcerative colitis patients were evaluated with invasive indices: the St. Mark's index and the Ulcerative Colitis Disease Activity Index (UCDAI); and noninvasive indices: the Simple Clinical Colitis Activity Index (SCCAI) and the Seo index. The correlations between the indices were measured. The contribution of the endoscopic items was measured with linear regression modeling. The overlap of endoscopy with other items in the standard indices was determined through factor analysis. RESULTS: The two noninvasive indices correlated well with the invasive St. Mark's Index (SCCAI 0.86, Seo 0.70). After adjusting for the three noninvasive UCDAI items, the UCDAI endoscopy item predicted only 0.04% of the variance in the St. Mark's index. Factor analysis demonstrated that this is because the endoscopy items in the invasive indices correlate with stool frequency and stool blood items. CONCLUSIONS: Endoscopy items contribute little additional information to indices of disease activity in ulcerative colitis. The clinical practice of treating patients based on reported symptoms is appropriate. The use of noninvasive indices in clinical trials could lower study costs and may increase subjects' willingness to participate.

Adult↗
PubMedDate not supplied

HLA antigens in ulcerative colitis and primary sclerosing cholangitis.

The aims of this study were to find out whether the alleles of the HLA class I or II region are associated with susceptibility to ulcerative colitis, and to show whether there is a difference or similarity in HLA associations between primary sclerosing cholangitis and ulcerative colitis. HLA-A, B, C and DR antigens were studied using the standard lymphocyte microcytotoxicity test in 24 Finnish patients with primary sclerosing cholangitis, 77 patients with ulcerative colitis, and 106 controls. HLA-B8 (54%) and DR3 (60%) were associated with primary sclerosing cholangitis. HLA-DR1 (46%) and DR6 (20%) seemed more common in ulcerative colitis than in controls. A positive association with Cw7 was common to both ulcerative colitis (25%) and primary sclerosing cholangitis (33%). Our results indicate that ulcerative colitis is more heterogeneous than primary sclerosing cholangitis in its HLA-DR associations.

Adolescent↗
PubMed1995

Effects of chronic nitric oxide synthase inhibition on TNB-induced colitis in rats.

Nitric oxide (NO) synthesis is increased in ulcerative colitis, but the role of NO in colitis is poorly understood. The present study employed Nw-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, in rats to evaluate the effect of NO on 2,4,6-trinitrobenzenesulphonic acid (TNB)-induced colitis. L-NAME solutions were placed in subcutaneous, osmotic mini-pumps which continuously released L-NAME at 0.042, 0.208, 0.417, or 1.667 mg kg-1 h-1. L-NAME dose-dependently enhanced lesions in TNB-induced colitis. The two higher doses of L-NAME significantly increased colonic mucosal damage, although there was slight, nonsignificant reduced lesion formation with the lowest dose of L-NAME. 0.042 mg kg-1 h-1. A single dose of L-NAME at 100 mg kg-1 subcutaneously injected daily in TNB-treated rats also increased lesions, and these ulcerogenic actions of L-NAME were reversed by L-arginine but not by D-arginine (both at 500 mg kg-1, s.c.). Only the highest dose of L-NAME (mini-pump) significantly depressed myeloperoxidase (MPO) activity. Faecal occult bleeding showed a close relationship with severity of colitis. These findings suggest that there may exist a balance between NO protective and aggressive effects. In TNB-induced colitis, antagonism of endogenous NO generation was intensified, whereas slight inhibition of NO synthesis reduced lesions. Variations in responses, related to timing or dose changes in L-NAME, may reflect the differences in inducible vs constitutive NO synthase isoforms.

Animals↗
PubMed2004

Interleukin 1beta-induced production of H2O2 contributes to reduced sigmoid colonic circular smooth muscle contractility in ulcerative colitis.

We have shown that neurokinin A-induced contraction of human sigmoid circular muscle (HSCM) is reduced in patients with ulcerative colitis and that interleukin (IL)-1beta may play a role in this change. We now examine changes in the signal transduction pathway mediating neurokinin A-induced contraction of HSCM and explore the role of IL-1beta and of H(2)O(2) in these changes. In Fura 2-AM-loaded ulcerative colitis HSCM cells, neurokinin A- and caffeine-induced peak Ca(2+) increase and cell shortening were significantly reduced. In normal cells, neurokinin A-induced contraction was decreased by protein kinase C inhibitor chelerythrine and by calmodulin inhibitor CGS9343B [1,3-dihydro-1-[1-[(4-methyl-4H,6H-pyrrolo[1,2-a][4,1]-benzoxazepin-4-yl)methyl]-4-piperidinyl]-2H-benzimidazol-2-one (1:1) maleate]. In ulcerative colitis muscle cells, contraction was inhibited only by chelerythrine but not by CGS9343B. IL-1beta treatment of normal HSCM strips and cells reproduced the changes observed in ulcerative colitis. IL-1beta-induced reduction in caffeine-induced peak Ca(2+) increase and contraction was reversed by catalase, suggesting a role of H(2)O(2). IL-1beta-induced H(2)O(2) production was inhibited by mitogen-activated protein kinase (MAPK) kinase inhibitor PD98059 (2'-amino-3'-methoxyflavone) and by cytosolic phospholipase A2 (cPLA(2)) inhibitor AACOCF3 (arachidonyltrifluoromethyl ketone), but neither by p38 MAPK inhibitor SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole] nor by nuclear factor-kappaB (NF-kappaB) inhibitory peptide NF-kappaB SN50 (H-Ala-Ala-Val-Ala-Leu-Leu-Pro-Ala-Val-Leu-Leu-Ala-Leu-Leu-Ala-Pro-Val-Gln-Arg-Lys-Arg-Gln-Lys-Leu-Met-Pro-OH). IL-1beta significantly increased the phosphorylation of extracellular signal-regulated kinase 1 (ERK1)/ERK2 MAPKs and cPLA(2) and IL-1beta-induced cPLA(2) phosphorylation was blocked by PD98059. We conclude that Ca(2+) stores of HSCM cells may be reduced in ulcerative colitis and that the signal transduction pathway of neurokinin A-induced contraction switches from calmodulin- and protein kinase C-dependent in normal cells to protein kinase C-dependent in ulcerative colitis cells. IL-1beta reproduces these changes, possibly by production of H(2)O(2) via sequential activation of MAPKs (ERK1/ERK2) and cPLA(2).

Calcium↗
PubMed2006

Escherichia coli strain Nissle 1917 ameliorates experimental colitis via toll-like receptor 2- and toll-like receptor 4-dependent pathways.

Toll-like receptors (TLRs) are key components of the innate immune system that trigger antimicrobial host defense responses. The aim of the present study was to analyze the effects of probiotic Escherichia coli Nissle strain 1917 in experimental colitis induced in TLR-2 and TLR-4 knockout mice. Colitis was induced in wild-type (wt), TLR-2 knockout, and TLR-4 knockout mice via administration of 5% dextran sodium sulfate (DSS). Mice were treated with either 0.9% NaCl or 10(7) E. coli Nissle 1917 twice daily, followed by the determination of disease activity, mucosal damage, and cytokine secretion. wt and TLR-2 knockout mice exposed to DSS developed acute colitis, whereas TLR-4 knockout mice developed significantly less inflammation. In wt mice, but not TLR-2 or TLR-4 knockout mice, E. coli Nissle 1917 ameliorated colitis and decreased proinflammatory cytokine secretion. In TLR-2 knockout mice a selective reduction of gamma interferon secretion was observed after E. coli Nissle 1917 treatment. In TLR-4 knockout mice, cytokine secretion was almost undetectable and not modulated by E. coli Nissle 1917, indicating that TLR-4 knockout mice do not develop colitis similar to the wt mice. Coculture of E. coli Nissle 1917 and human T cells increased TLR-2 and TLR-4 protein expression in T cells and increased NF-kappaB activity via TLR-2 and TLR-4. In conclusion, our data provide evidence that E. coli Nissle 1917 ameliorates experimental induced colitis in mice via TLR-2- and TLR-4-dependent pathways.

Animals↗
PubMed1974

Properties of strains of Escherichia coli carried in different phases of ulcerative colitis.

Strains of E. coli from the faeces of patients with active ulcerative colitis and with colitis in remission were examined for haemolysin and necrotoxin production. Cultures from 63 patients with active colitis grew haemolytic E. coli in 23 (37%) as compared with 24 (21%) from 115 patients whose disease was in remission (p < 0.05). The corresponding proportions for necrotoxin-producing strains were 22% and 12%. Of 35 patients investigated both in relapse and remission of the colitis, 14 changed their carriage of haemolytic E. coli. Thirteen of these carried haemolytic organisms in relapse but not in remission, and one carried haemolytic organisms in remission but not in relapse (p < 0.01). Strains of E. coli were also examined from specimens of faeces obtained at weekly intervals for 28 weeks from 19 patients. The acquisition of haemolytic or necrotoxic E. coli strains tended to follow rather than precede the onset of the attack in the four patients who developed a relapse of the disease during this period. Among these 19 patients haemolytic and necrotoxic strains were found most commonly when blood was regularly present in the faeces. These facts suggest that conditions in the bowel during a relapse of colitis tend to favour the presence of haemolysin- and necrotoxin-producing organisms, rather than that these organisms cause the relapse. Of 50 strains of E. coli from patients treated with sulphasalazine tested for sensitivity to sulphapyridine 49 were resistant. There was no clear relation between the activity of the colitis and the presence of any of the 27 serotypes of E. coli examined.

Colitis, Ulcerative↗