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PubMed2006

Adoptive transfer of nontransgenic mesenteric lymph node cells induces colitis in athymic HLA-B27 transgenic nude rats.

HLA-B27 transgenic (TG) rats develop spontaneous colitis when colonized with intestinal bacteria, whereas athymic nude (rnu/rnu) HLA-B27 TG rats remain disease free. The present study was designed to determine whether or not HLA-B27 expression on T cells is required for development of colitis after transfer of mesenteric lymph node (MLN) cells into rnu/rnu HLA-B27 recipients. Athymic nontransgenic (non-TG) and HLA-B27 TG recipients received MLN cells from either TG or non-TG rnu/+ heterozygous donor rats that contain T cells. HLA-B27 TG rnu/rnu recipients receiving either non-TG or TG MLN cells developed severe colitis and had higher caecal MPO and IL-1beta levels, and their MLN cells produced more IFN-gamma and less IL-10 after in vitro stimulation with caecal bacterial lysate compared to rnu/rnu non-TG recipients that remained disease free after receiving either TG or non-TG cells. Interestingly, proliferating donor TG T cells were detectable one week after adoptive transfer into rnu/rnu TG recipients but not after transfer into non-TG recipients. T cells from either non-TG or TG donors induce colitis in rnu/rnu TG but not in non-TG rats, suggesting that activation of effector T cells by other cell types that express HLA-B27 is pivotal for the pathogenesis of colitis in this model.

Adoptive Transfer↗
PubMed1996

Expression of nitric oxide synthase in ulcerative colitis.

Nitric oxide (NO) is generated from L-arginine by a family of enzymes called the NO synthases. Previous investigators have proposed that the expression of this inducible enzyme (iNOS) may account for the characteristic vasodilatation, oedema and impairment of get motility seen in active ulcerative colitis. Using a specific antibody to iNOS, we have investigated the distribution of this enzyme in colonic tissue from patients with histologically proven ulcerative colitis. Eight patients with ulcerative colitis expressed calcium-independent citrulline activity (9.96 +/- 2.34 pmol citrulline mg-1 protein min-1) and showed immunoreactivity to the iNOS antibody within the inflammatory infiltrate of the lamina propria, and also within the cytoplasm of the epithelial cells lining the colon. Five age-matched controls showed no calcium-independent citrulline activity (0.2 +/- 0.08 pmol citrulline mg-1 protein min-1) and no immunoreaction to the antibody. We conclude that this enzyme is present in colonic tissue including the epithelium from patients with active colitis. Inhibition of this enzyme may provide a novel therapeutic option for patients with active ulcerative colitis.

Adult↗
PubMed2005

Sodium alginate as a novel therapeutic option in experimental colitis.

The potential therapeutic effect of low-viscosity sodium alginate (LVA) was studied in a rat model of acute colitis induced by intracolonic administration of acetic acid. This experimental model produced a significant ulcerative colitis. Induction of colitis also significantly enhanced the serum and colonic mucosal cytokine (IL-6 and TNF-alpha) and eicosanoid (LTB4 and PGE2) levels, which paralleled with the severity of colitis. LVA solution was administered orally as drinking water at concentration of 0.5% (W/V) for 1 week. The tolerability and inhibitory effect of LVA on matrix metalloproteinase-2 (MMP-2) were tested using WEHI-164 cell line and zymography method. The results showed that LVA therapy is able to significantly reduce colonic damage score, histological lesion, serum and colonic mucosal IL-6, TNF-alpha, LTB4 and PGE2 levels in treated group compared with nontreated controls. Moreover, in vitro examinations revealed that treatment with LVA could diminish MMP-2 activity. It is concluded that LVA is able to suppress acetic acid-induced colitis in rats. Some of the action of LVA may be associated with its inhibitory effects on cytokine and eicosanoid production and MMP-2 activity. Our data suggest that LVA could potentially be a novel therapeutic option for inflammatory bowel disease.

Alginates↗
PubMed2006

Probiotics modulate inflammatory cytokine secretion from inflamed mucosa in active ulcerative colitis.

Enteric microflora of ulcerative colitis patients becomes aberrant. The abnormal interaction between microflora and intestinal mucosal immune system leads the mucosal inflammation. Probiotic administration may recover the commensal microflora and normalise the host-microbial interaction. In this experiment, we cocultured colonic biopsies from active ulcerative colitis patients with bifidobacterium to investigate the modulation effect of probiotics on inflamed colonic tissues and its possible mechanism. Colonic biopsies from active ulcerative colitis were cocultured for 24 h with Bifidobacterium longum. Tumour necrosis factor (TNF)-alpha and interleukin (IL)-8 in supernatants were measured using enzyme-linked immunosorbent assays, the biopsies were fixed using paraffin and the expression of NF-kappaB P65 of tissues was studied using immunohistochemical staining. The concentrations of TNF-alpha and IL-8 in supernatants of tissues cocultured with probiotics were lower than those cultured alone. The number of lamina propria mononuclear cells (LPMC) with nuclear factor-kappa B (NF-kappaB) P65 positive in cocultured tissues was also decreased. When cocultured with inflamed tissues of active ulcerative colitis, probiotics could inhibit NF-kappaB activation in LPMC and down-regulate inflammatory cytokine secretion from inflamed tissues of active ulcerative colitis.

Adolescent↗
PubMed2006

Distribution of signal transducer and activator of transcription 6 gene G2964A polymorphism in Chinese patients with ulcerative colitis.

BACKGROUND AND AIMS: The signal transducer and activator of transcription 6 (STAT6) gene is located on chromosome 12q13.3-14.1 just within the IBD2 region and is a key transcription factor involved in interleukin (IL)-4 and IL-13-mediated Th2 response. The aim of the present study was to determine distribution of the STAT6 gene polymorphism in Chinese patients with ulcerative colitis. METHODS: The G2964A polymorphism in the 3' untranslated region of the STAT6 gene was studied in 84 unrelated Chinese patients with ulcerative colitis and 176 healthy controls by PCR and the amplification created restriction site method. The results were then compared with those from a Dutch study published previously. RESULT: Significant differences in genotype and allele frequencies of the STAT6 G2964A polymorphism were not found between patients with ulcerative colitis and healthy controls. Subgroups of the patients with ulcerative colitis classified according to the age at onset, sex and location of disease did not differ significantly in the distribution of this polymorphism. However, the genotypes (P < 0.0001, chi-squared = 75.332) and allele frequencies (P < 0.0001, odds ratio = 4.298, 95% confidence interval = 3.070-6.018) were significantly different between the Chinese and Dutch populations. CONCLUSION: The STAT6 G2964A polymorphism is not involved in the genetic susceptibility to ulcerative colitis in Chinese patients.

Adult↗
PubMed1999

Commonalities in the time trends of Crohn's disease and ulcerative colitis.

OBJECTIVE: The analysis of the time trends of inflammatory bowel disease (IBD) is a powerful research tool to assess the contribution of environmental factors to its etiology and to gain insights about possible causative mechanisms. A previous study revealed a characteristic relationship between the time trends of mortality from Crohn's disease and ulcerative colitis. The present study aimed to test whether the most recent temporal patterns still corroborate the hypothesis of two interacting risk factors in the development of IBD. The time trends of IBD from six countries were checked for common features. METHODS: Mortality data from Australia, Canada, England and Wales, the Netherlands, Sweden, and the United States were analyzed. Age- and sex-specific death rates, as well as total death rates, from Crohn's disease and ulcerative colitis were plotted against the period of death. RESULTS: Mortality from ulcerative colitis decreased continuously during the past 40 years. Mortality from Crohn's disease increased between 1950 and the mid-1970's until reaching a similar level as mortality from ulcerative colitis. Since then the death rates of both diseases have followed a parallel time course. A similar behavior was found, if male and female data were analyzed separately. It could be also discerned in the time trends of each age group. The data from all six countries revealed identical temporal patterns. CONCLUSIONS: The similar time trends of IBD from different countries support the hypothesis that identical causative mechanisms are responsible for the mortality and the occurrence of IBD among populations characterized by different political history and health care systems. The rapidity of the temporal changes implicates environmental agents in the etiology of both diseases. The relationships between the temporal changes of Crohn's disease and ulcerative colitis point at the existence of a shared risk factor responsible for the occurrence of both diseases, and at the existence of at least one additional factor, responsible for the expression of Crohn's disease alone.

Adult↗
PubMed2001

Dietary inulin improves distal colitis induced by dextran sodium sulfate in the rat.

OBJECTIVES: Inulin stimulates intracolonic generation of butyrate and growth of lactic acid bacteria. This study investigated whether inulin protects against colitis. METHODS: Rats with dextran sodium sulfate colitis received inulin either orally (1% in drinking water, or 400 mg/day) or by enema. Matched groups received vehicle. In addition, fecal water obtained from inulin-fed rats was administered by enema to rats with colitis and compared with fecal water from control rats. Finally, rats with colitis received daily enemas of either butyrate (at 40 or 80 mmol/L) or vehicle. Inflammation was assessed by eicosanoid asssay in rectal dialysates and MPO activity in colonic tissue. Mucosal lesions were blindly scored by microscopic examination. Luminal pH was measured from cecum to rectum by a surface microelectrode. RESULTS: Oral inulin prevented inflammation, as evidenced by lower lesion scores (p < 0.05), decreased release of mediators (p < 0.05), and lower tissue MPO (p < 0.05) as compared with controls. Inulin induced acidic environment (pH <7.0) from cecum to left colon and increased counts of lactobacilli. Fecal water from inulin-fed rats also reduced scores (p < 0.05) and inflammation (p < 0.05). However, inulin or butyrate enemas had no effect. CONCLUSIONS: Oral inulin reduces the severity of dextran sodium sulfate colitis. The effect seems to be mediated by modification of the intracolonic milieu.

Animals↗
PubMed2002

High prevalence of undetected ulcerative colitis: data from the Nottingham fecal occult blood screening trial.

OBJECTIVES: Inflammatory bowel disease (IBD) is usually diagnosed as a result of symptoms but occasionally is found during investigation for other conditions. An earlier report from Nottingham had found a high prevalence of previously undetected "asymptomatic" IBD detected as a result of colorectal cancer screening, and the aim of this study was to reassess the prevalence, symptoms, and outcome in these patients. METHODS: We investigated subjects found to be fecal occult blood (FOB) positive in a randomized trial of FOB screening for colorectal cancer. All FOB-positive subjects were investigated by colonoscopy or flexible sigmoidoscopy and barium enema. Subjects with IBD were referred back to their general practitioner for any further investigation and treatment. RESULTS: Seventy-five thousand two hundred fifty-three subjects (aged 45-74) were sent FOB tests and 44,838 (60%) completed a series of tests on one or more occasions. Of 133,000 test series, 1.5% were positive. During investigation 53 cases of previously undetected IBD (52 of ulcerative colitis) were found; 52% (27/52) had proctosigmoiditis only, whereas 25% (13/52) had pancolitis. Only 17% (9/52) were completely asymptomatic, with a half or more reporting some rectal bleeding (54%) or diarrhea (50%). The overall prevalence of undetected ulcerative colitis was 69/10(5) (95% CI = 50-88/10(5)) in people offered screening and 116/10(5) (95% CI = 85-147/10(5)) in people accepting screening and was higher in men. Of 32 subjects followed up 2-12 yr after diagnosis, 91% (29) continued to have few or no symptoms, with only 12 currently receiving any treatment for their colitis. CONCLUSIONS: In comparison with detected disease, undetected ulcerative colitis is relatively common but does usually cause some symptoms. It generally appears to follow a benign course, but a significant proportion have extensive colitis and may therefore be at an increased risk of colorectal cancer.

Age Distribution↗
PubMed2002

Focally enhanced gastritis in children with Crohn's disease and ulcerative colitis.

OBJECTIVES: Focally enhanced gastritis (FEG) has been suggested as a specific diagnostic marker for patients with Crohn's disease. However, the utility of FEG for distinguishing Crohn's disease from ulcerative colitis is uncertain in adults, and the occurrence of this lesion in children has not been defined. The aim of this study was to evaluate the occurrence of FEG and other gastric histological abnormalities in children with inflammatory bowel disease (IBD) and to examine the utility of FEG in discriminating between ulcerative colitis and Crohn's disease. METHODS: This is a retrospective, case-controlled study of upper GI histopathological findings in children with IBD. Gastric histopathology was defined and graded according to the Updated Sydney System. RESULTS: FEG was present in 28 of 43 (65.1%) children with Crohn's disease and five of 24 (20.8%) children with ulcerative colitis, compared to three of 132 (2.3%) children without IBD or one of 39 (2.6%) children with Helicobacter pylori infection. There were no differences between those with and without FEG with regard to upper GI symptoms or previous anti-inflammatory drug ingestion (5-aminosalicylic acid compounds or steroids). All patients with H. pylori infection had chronic antral gastritis, but only one child with H. pylori had FEG. In addition, mild to moderate chronic gastritis was present in 15 of 43 (34.9%) children with Crohn's disease and in 12 of 24 (50%) patients with ulcerative colitis. CONCLUSIONS: The presence of FEG suggests underlying IBD. Although FEG is particularly common in children with Crohn's disease, it does not reliably differentiate between Crohn's disease and ulcerative colitis.

Case-Control Studies↗
PubMed2002

The long-term time trends of peptic ulcer and ulcerative colitis are interrelated.

OBJECTIVE: A birth-cohort phenomenon in the time trends of a disease indicates that exposure to relevant risk factors must have occurred during an early period of life. The aim of this study was to determine whether birth-cohort patterns are common features of ulcerative colitis, gastric ulcer, and duodenal ulcer in different countries. METHODS: The number of deaths from ulcerative colitis, gastric, and duodenal ulcer in England, Netherlands, Italy, Switzerland, United States, and Scotland were retrieved from the respective national statistics offices. The death rates from the six countries were plotted against the period of birth. Age-standardized cohort mortality ratios were calculated as a summary of the overall mortality associated with each consecutive birth-cohort. RESULTS: In all countries alike, mortality from ulcerative colitis, gastric, and duodenal ulcer increased among successive generations born during the 19th century and, after reaching a sharp peak around the turn of the 20th century, declined among generations born subsequently. The rise in mortality from gastric ulcer preceded a similar rise in mortality from duodenal ulcer by 10-20 yr, and the temporal changes of duodenal ulcer coincided with those of ulcerative colitis. CONCLUSIONS: The sudden rise of peptic ulcer disease during the 19th century and the 10-20-yr time lag between gastric and duodenal ulcer are difficult to explain based on changing infection rates with Helicobacterpylori alone. The similarity between the time trends of duodenal ulcer and ulcerative colitis suggests the influence of one or more shared risk factors.

Adult↗
PubMed2002

Lansoprazole-associated microscopic colitis: a case series.

Lansoprazole is a potent proton pump inhibitor that has been well tolerated with minimal serious adverse events. One of the most commonly reported side effects is diarrhea in 3-8% of study patients. During 1997, approximately 850 veterans at our institution had their proton pump inhibitor converted from omeprazole to lansoprazole because of a formulary change. A number of patients subsequently developed chronic watery diarrhea. While evaluating six of these patients, we discovered microscopic colitis that resolved with discontinuation of lansoprazole. The diarrhea was described as three to 10 loose, nonbloody bowel movements per day with some abdominal cramping. Colonoscopy in five patients and flexible sigmoidoscopy in one patient revealed normal colonic mucosa, but random biopsies all supported microscopic colitis (five cases of lymphocytic colitis and one case of collagenous colitis). Complete symptom resolution occurred in all patients within 4 to 10 days of discontinuing lansoprazole. In all patients, follow-up biopsies demonstrated normalization of the colonic histology. This is the first published case series of patients with microscopic colitis that correlated clinically and histologically with the initiation and discontinuation of lansoprazole.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2003

Abnormal p53 immunohistochemistry is associated with an increased colorectal cancer-related mortality in patients with ulcerative colitis.

OBJECTIVE: Immunohistochemical evaluation of p53 staining patterns has been considered as a complementary test for dysplasia in ulcerative colitis-related colorectal cancer surveillance, but usefulness would be particularly important if it were a marker associated with a poor prognosis. The aim of this study was to determine whether abnormal p53 staining of the tumor correlated with cancer-related mortality in ulcerative colitis patients. METHODS: An historical cohort study was designed to examine all ulcerative colitis patients who developed colorectal cancer between 1978 and 1997 and who had tumor tissue blocks available for staining. Tissue was recut and stained for abnormal p53 immunohistochemistry using the DO-7 antibody. Tumors were considered to be p53 positive if at least 5% of nuclei in a high power field were positive for staining. RESULTS: Among 75 patients entered in the study, 38 (50.7%) had p53 positive tumors. Fourteen patients (36.8%) with p53 positive tumors died from colorectal cancer, compared to five (13.5%) with p53 negative tumors (p < 0.04, log-rank test). The adjusted relative risk of cancer-related death among patients with p53 positive tumors was 3.03 (95% CI = 1.05-8.73). CONCLUSIONS: Abnormal p53 immunohistochemistry of tumors is associated with a poor prognosis among ulcerative colitis patients who develop colorectal cancer. As such, p53 immunohistochemical staining could be a useful histological marker to complement routine histology in cancer surveillance programs in ulcerative colitis patients.

Adolescent↗
PubMed2006

Acutely administered melatonin is beneficial while chronic melatonin treatment aggravates the evolution of TNBS-induced colitis.

The aim of this study was to evaluate the effects of melatonin on the inflammatory response and hydroxyproline production in an experimental acute and chronic model of trinitrobenzene sulfonic (TNBS) acid-induced colitis in Wistar rats. In the acute model, melatonin (0.5, 1, and 2 mg/kg, i.p.) was applied 48, 24, and 1 hr prior to the induction of colitis and 24 and 48 hr after; the severity of colitis was less evident in melatonin-treated animals with significant response in the group treated with 2 mg/kg. All doses investigated significantly reduced the myeloperoxidase activity (MPO). In the chronic studies, melatonin (1 and 2 mg/kg, i.p.) was administered daily 24 hr before hapten instillation and for 7 or 21 days after TNBS; melatonin (2 mg/kg) worsened colitis evolution in the 21-day study with a significant increase in MPO activity and tumor necrosis factor-alpha production with respect to TNBS group. Histological slides were in concordance with macroscopic data where areas of extensive necrosis and edema, fibrosis, and absence of regenerated epithelium were observed. Moreover, the hydroxyproline determination, used as indicator of collagen production and fibrosis, also showed a marker increase. The results obtained in this experimental model showed that short-term administration is protective while in the long term it negatively influences evolution of inflammatory colitis; therefore, the immunostimulatory effect of melatonin in some situations when given chronically, such as during inflammatory bowel disease, might lead to negative consequences.

Animals↗
PubMed1986

Colitis: differential diagnosis and treatment.

Equine colitis characterised by diarrhoea and/or pain may be caused by a wide variety of bacterial, viral, protozoal agents and toxins. The causative agent of Potomac horse fever, Ehrlichia risticii, is the most recently recognised cause of colitis. Salmonella, the agent typically associated with colitis, also causes abdominal pain (colic) of variable intensity. Acute colitis is also caused by colitis X, various antibiotics, endotoxic shock and peritonitis caused by arterial infarction. The principles of therapy for each of these, together with means of differential diagnosis, are presented.

Animals↗
PubMed2003

Hepatocyte growth factor facilitates colonic mucosal repair in experimental ulcerative colitis in rats.

Hepatocyte growth factor (HGF) modulates intestinal epithelial cell proliferation and migration, serving as a critical regulator of intestinal wound healing. In this study, we examined the effect of administration of recombinant human HGF on colonic mucosal damage in vivo. Acute colitis was induced in rats by feeding with 5% dextran sulfate sodium (DSS) for 7 days, and colitis was subsequently maintained by feeding with 1% DSS. On the 5th day of DSS administration, osmotic pumps releasing recombinant human HGF (200 microg/day) were implanted into the peritoneum of the rats. Continuous intraperitoneal delivery of HGF led to both increased serum human HGF levels and c-Met tyrosine phosphorylation within the colonic mucosa. Compared with mock-treated rats, those administered human HGF showed a reduction in colitis-associated weight loss, large intestinal shortening, and improved colonic erosions. Enhanced epithelial regeneration and cellular proliferation were observed in rats treated with recombinant human HGF. The weights of the liver, kidneys, and spleen were not affected by HGF administration. These results indicate that HGF administration accelerates colonic mucosal repair in rats with DSS-induced colitis and suggest that recombinant human HGF may be a useful therapeutic tool to facilitate intestinal wound healing in patients with ulcerative colitis.

Animals↗
PubMed2006

Epithelial toll-like receptor 5 is constitutively localized in the mouse cecum and exhibits distinctive down-regulation during experimental colitis.

We recently demonstrated that the pattern recognition receptors (PRRs) toll-like receptor 2 (TLR2), TLR4, and CD14 are expressed in mouse colonic epithelium in a compartmentalized manner. Here we report the localization of TLR5, the receptor for bacterial flagellin, and its distinctive down-regulation during experimental colitis. Guts from normal BALB/c mice and those with dextran sodium sulfate (DSS)-induced colitis were compared. Each gut was divided into seven segments (stomach, small intestine [three parts], and colon [three parts]), and epithelial cells and crypt units were collected by scraping and EDTA treatment, respectively. Northern blotting showed that TLR5 mRNA was preferentially expressed in the epithelium of the proximal colon in normal mice. Laser capture microdissection coupled to reverse transcriptase PCR confirmed this localization. TLR5 protein expression reflected mRNA expression, as evidenced by Western blotting. In mice with acute colitis, inflammation occurred mainly in the distal colon. Interestingly, while TLR2, TLR4, and CD14 were up-regulated in the inflamed colon, TLR5 was down-regulated at both the mRNA and protein levels. Decreased TLR5 expression was more evident during chronic colitis. Additional in vitro studies using a mouse cell line, Colon-26, showed that gamma interferon (IFN-gamma) time- and dose-dependently down-regulates TLR5. In conclusion, epithelial cells, mainly in the proximal colon, constitutively express TLR5. TLR5 expression is down-regulated in vivo during acute and chronic DSS-induced colitis, in contrast to the expression of TLR2, TLR4, and CD14. The mechanism governing TLR5 regulation may therefore differ from that controlling other PRRs. Finally, IFN-gamma may be involved in down-regulating TLR5 expression.

Animals↗
PubMed2006

Chronic Salmonella enterica serovar Typhimurium-induced colitis and cholangitis in streptomycin-pretreated Nramp1+/+ mice.

Salmonella enterica subspecies 1 serovar Typhimurium is an enteric bacterial pathogen infecting a broad range of hosts. In susceptible Nramp1(-/-) (Slc11alpha1(-/-)) mice, serovar Typhimurium cannot efficiently colonize the intestine but causes a systemic typhoid-like infection. However, after pretreatment with streptomycin, these susceptible (C57BL/6 and BALB/c) mice develop acute serovar Typhimurium-induced colitis (M. Barthel et al., Infect. Immun. 71:2839-2858, 2003). It was not clear whether resistant Nramp1(+/+) (Slc11alpha1(+/+)) mouse strains would similarly develop colitis. Here we compared serovar Typhimurium infection in streptomycin-pretreated susceptible (C57BL/6) and resistant (DBA/2 and 129Sv/Ev) mouse strains: We found that acute colitis (days 1 and 3 postinfection) is strikingly similar in susceptible and resistant mice. In 129Sv/Ev mice we followed the serovar Typhimurium infection for as long as 6 weeks. After the initial phase of acute colitis, these animals developed chronic crypt-destructive colitis, including ulceration, crypt abscesses, pronounced mucosal and submucosal infiltrates, overshooting regeneration of the epithelium, and crypt branching. Moreover, we observed inflammation of the gall duct epithelium (cholangitis) in the 129Sv/Ev mice between days 14 and 43 of infection. Cholangitis was not attributable to side effects of the streptomycin treatment. Furthermore, chronic infection of 129Sv/Ev mice in a typhoid fever model did not lead to cholangitis. We propose that streptomycin-pretreated 129Sv/Ev mice provide a robust murine model for chronic enteric salmonellosis including complications such as cholangitis.

Animals↗
PubMed1999

Differential induction of colitis and gastritis in HLA-B27 transgenic rats selectively colonized with Bacteroides vulgatus or Escherichia coli.

Resident bacteria play an important role in initiating and perpetuating gastrointestinal inflammation. We previously demonstrated that six commensal bacteria including Bacteroides vulgatus caused more aggressive colitis and gastritis in HLA-B27 transgenic rats than did the other five bacteria without B. vulgatus. This study compared the degree of gastrointestinal inflammation in gnotobiotic HLA-B27 transgenic rats monoassociated with either B. vulgatus or Escherichia coli. Gnotobiotic transgenic rats raised in Trexler isolators were selectively colonized with either B. vulgatus or E. coli. Control rats were either germfree or colonized with six common commensal bacteria (Streptococcus faecium, E. coli, Streptococcus avium, Eubacterium contortum, Peptostreptococcus productus, and B. vulgatus [DESEP-B]). After 1 month, all the rats were killed and tissues were prepared for histologic and biochemical evaluation. Colitis induced by B. vulgatus monoassociation was almost equal to that in DESEP-B-colonized rats and was significantly more severe than E. coli-induced colitis, which was absent by histological testing and mild by colonic myeloperoxidase and interleukin-1beta concentration determinations. However, gastritis was detectable only in DESEP-B-associated rats. These studies suggest that not all resident bacteria have equal proinflammatory capabilities, since B. vulgatus alone is more active than E. coli alone in inducing colitis, and that colitis and gastritis result from different luminal bacterial stimuli.

Animals↗