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PubMed1989

Lipoxygenase metabolites of arachidonic acid do not induce mucus secretion from rabbit intestinal goblet cells in vitro.

Lipoxygenase metabolites of arachidonic acid are effective mucus secretagogues in the respiratory tract but their efficacy in the intestinal tract was unknown. Mucosal explants and sheets of epithelial cells isolated from rabbit small and large intestine were exposed to leukotrienes B4, C4, and D4 and monohydroxyeicosatetraenoic acids 5-HETE, 12-HETE, and 15-HETE. Light and electron microscopic inspection of goblet cells in treated tissues failed to detect evidence of recent compound exocytosis of mucin granules or other morphological evidence of secretory activity. These results indicate that lipoxygenase metabolites are not directly responsible for the increased mucus secretion observed in ulcerative colitis.

Animals↗
PubMed1996

Rapid identification of patient specimens with microsatellite DNA markers.

Despite the use of standardized clerical and processing procedures in surgical pathology, questions might arise regarding the proper identification of specimens with respect to patient source. Genotypic analysis of microsatellite DNA polymorphisms was used to identify the patient source of two surgical pathology specimens showing carcinoma. Four highly polymorphic microsatellite loci were evaluated in DNA extracted from various formalin-fixed, paraffin-embedded tissues. Using this technique, we determined that the diagnosis of poorly differentiated adenocarcinoma arising from a background of colitis had been assigned to the correct patient, despite the fact that multiple repeat endoscopic examinations, with biopsy specimens, were negative. In the second case, a suspected processing error involving the exchange of specimen accession numbers was resolved when a lymph node containing a microscopic focus of metastatic carcinoma was assigned to the appropriate patient. A multitude (approximately 50,000 to 100,000) of microsatellite loci are distributed throughout the human genome, and many are highly polymorphic. Hence, genotypic analysis using microsatellite loci has a significantly higher power of discrimination than other commonly used methods. The technique is rapid and is particularly well suited to the analysis of small, fixed-tissue specimens.

Adenocarcinoma↗
PubMed2004

Inhibitory effects of etodolac, a selective COX-2 inhibitor, on the occurrence of tumors in colitis-induced tumorigenesis model in rats.

Ulcerative colitis (UC)-associated neoplasia is one of the complications seen in patients with long-standing UC. Based on many epidemiological studies, colitis is assumed to promote colon tumorigenesis. Tumorigenesis is known to be suppressed in rodents and humans by selective cyclooxygenase-2 inhibitors. However, whether these drugs would serve as protective agents against UC-associated neoplasia remains unclear. Therefore, using a colitis-induced tumorigenesis rat model, we investigated the effects of etodolac, a selective cyclooxygenase-2 inhibitor, on tumorigenesis. The following 4 groups were examined: group A, administered trinitrobenzene sulfonic acid and 1,2-dimethylhydrazine; group B, in addition to the treatment in group A, also received etodolac; group C, administered etodolac alone; and group D, did not receive any agent throughout the study and served as an untreated control. The rats were sacrificed 163 days after the start of experiment, and the number of aberrant crypt foci and tumors in the intestine were counted using a stereoscopic microscope following methylene blue staining. The mean number of aberrant crypt foci was 52.4 in group A, 18.9 in group B, 0 in group C and 0.5 in group D. A total of 9 tumors were observed in group A alone, with none in the remaining groups. The numbers of aberrant crypt foci and tumors in group B were significantly lower than in group A. Etodolac, a selective cyclooxygenase-2 inhibitor, suppresses the occurrence of aberrant crypt foci and tumors in colitis-induced tumorigenesis in rats.

Animals↗
PubMed1997

Effect of Z-103 on TNB-induced colitis in rats.

Z-103 is a chelate compound consisting of zinc ion and L-carnosine. In this study, we investigated the protective effect of Z-103 against colonic damage induced by 2,4,6-trinitrobenzene sulfonic acid (TNB) in rats. Colonic inflammation was induced by administering TNB dissolved in 50% ethanol (120 mg/ml) in male Wistar rats (total volume of 0.25 ml per rat) following a 48-hour fast. After the administration of TNB, Z-103 was given at a dose of 30 mg/kg per rat for 1 week. A second group of rats received sulfasalazine (SASP) at 300 mg/kg and a third group of rats received 30 mg/kg of ZnSO4 for 1 week. Colonic inflammation was assessed 1 week following TNB administration. Both macro- and microscopic evaluation showed that the inflammatory responses induced by TNB were reduced by treatment with Z-103, SASP and ZnSO4. The score (graded from 0 to 5 according to the macroscopic lesions) and colonic wet weight (distal 8 cm of the colon) were significantly decreased by treatment with Z-103, SASP and ZnSO4. The increase in thiobarbituric acid-reactive substances in the colonic mucosa following TNB administration were inhibited in the Z-103 and SASP groups. These results suggest that Z-103 is as effective against TNB-induced colitis as SASP.

Animals↗
PubMed2002

Lamina propria and circulating interleukin-6 in newly diagnosed pediatric inflammatory bowel disease patients.

OBJECTIVES: Understanding cytokine production patterns in early mucosal lesions of pediatric patients newly diagnosed with inflammatory bowel disease (IBD) may be critical to understanding IBD pathogenesis. Interleukin-6 (IL-6) has a central role in a multitude of immune system reactions; however, inconsistent lamina propria and serum IL-6 has been reported in IBD patients. Newly diagnosed pediatric IBD patients have not previously been evaluated for lamina propria or serum IL-6. METHODS: Serum and intestinal lamina propria biopsy whole organ culture supernatants were evaluated by ELISA for IL-6 obtained from newly diagnosed IBD patients, before initiation of immunomodulatory therapies. RESULTS: Levels of lamina propria IL-6 demonstrated significant correlation with graded severity of histological inflammation (p < 0.001). Log-transformed serum and organ culture IL-6 levels demonstrated significant correlation (p < 0.0001, R2 = 0.6226). Assigning a demarcation level of >400 pg/ml, serum IL-6 concentrations were a superior marker for the presence of microscopic intestinal inflammation than erythrocyte sedimentation rate (ESR), with a sensitivity of 82%, specificity of 100%, positive predictive value of 100%, and negative predictive value of 82%. When evaluating subtypes of IBD, serum IL-6 levels were correlated more significantly with active disease in ulcerative colitis patients (p = 0.01, R2 = 0.74) than in Crohn's disease patients (p = 0.21, R2 = 0.33). CONCLUSIONS: This study outlines graded production of IL-6 in intestinal lamina propria and serum of newly diagnosed pediatric IBD patients, confirming the presence of IL-6 in early IBD patients. In addition, serum IL-6 may be a good predictor of IBD in pediatric patients with suspected or newly diagnosed IBD.

Adolescent↗
PubMed2000

Spontaneously developing chronic colitis in IL-10/iNOS double-deficient mice.

Mice deficient in both inducible nitric oxide synthase (iNOS) and interleukin (IL)-10 (iNOS(-/-)/IL-10(-/-)) were created to examine the role of iNOS in spontaneously developing intestinal inflammation. IL-10(-/-)/iNOS(-/-) mice were compared with IL-10(-/-) (iNOS(+/+)) littermates over 6 mo. RT-PCR, Western blot analysis, and immunohistochemistry were performed to measure iNOS message and protein levels. Plasma nitrate/nitrite (NO(x)) levels were assessed by HPLC. Damage scores (macroscopic and microscopic) and granulocyte infiltration were assessed. At 3-4 wk, IL-10(-/-) and IL-10(-/-)/iNOS(-/-) mice had no signs of colonic inflammation or granulocyte infiltration. Plasma NO(x) levels were not different from controls. By 3-4 mo, IL-10(-/-) mice had increased damage scores and granulocyte infiltration concurrent with increased mRNA and protein synthesis (restricted to the epithelium) for iNOS in intestinal tissues but not other tissues. Plasma NO(x) levels increased fivefold. Interestingly, in the absence of iNOS induction or increased plasma NO(x), iNOS(-/-)/IL-10(-/-) mice had damage and granulocyte infiltration equivalent to those observed in IL-10(-/-) littermates. These data suggest that iNOS does not impact on the development or severity of spontaneous chronic inflammation in IL-10-deficient mice.

Age Factors↗
PubMed2000

Prostaglandin E2 inhibits lesion formation in dextran sodium sulphate-induced colitis in rats and reduces the levels of mucosal inflammatory cytokines.

Effects of rectally injected prostaglandin E2 (PGE2) in rats with dextran sodium sulphate (DSS)-induced colitis were investigated in terms of histopathology, local myeloperoxidase (MPO) activity, local mRNA expression of interleukin-1beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and growth-regulated gene produced/cytokine-induced neutrophil chemoattractant (GRO/CINC)-1, and secretion of TNF-alpha and GRO/CINC-1. In animals with no PGE2 treatment, DSS-induced erosion and ulceration were particularly severe in the rectum and extended to the proximal colon. Neutrophil infiltration was characteristically present in the lesions and surrounding mucosa. MPO activity at lesion sites was increased. IL-1beta and GRO/CINC-1 mRNA expression was increased, while TNF-alpha mRNA expression was significantly decreased. GRO/CINC-1 secretion was increased but a similar elevation of TNF-alpha was not detected. In the PGE2-treated group, lesion formation was inhibited grossly and microscopically. Neutrophil infiltration and MPO activity in and around lesions were lessened. The reduction in TNF-alpha mRNA expression and secretion was not affected by PGE2. The expression of mRNA for IL-1beta and GRO/CINC-1 was reduced, as was the secretion of GRO/CINC-1. As mRNA expression and secretion of cytokines in lesions of non-PGE2-treated animals was similar to that reported in human ulcerative colitis, rectal injection of PGE2 may prove to be an effective therapy.

Animals↗
PubMed2000

Development of dextran sulphate sodium-induced experimental colitis is suppressed in genetically mast cell-deficient Ws/Ws rats.

Ws/Ws rats have a small deletion of the c-kit gene, and are deficient in both mucosal-type mast cells (MMC) and connective tissue-type mast cells (CTMC). In the present study we investigated the role of intestinal MMC in the development of dextran sulphate sodium (DSS)-induced experimental colitis using Ws/Ws rats. Ws/Ws and control (+/+) rats were given a 3% DSS aqueous solution orally for 10 days, and the subsequent mucosal damage was evaluated macroscopically and histologically. The mucosal myeloperoxidase (MPO) activities and histamine levels were also measured. (i) DSS induced severe oedema and hyperaemia with sporadic erosions in the control (+/+) rats, but these changes were significantly attenuated in the Ws/Ws rats (P < 0.01). (ii) The microscopic mucosal damage score was lower in the Ws/Ws rats than in the control (+/+) rats (P = 0.06). (iii) There were no significant differences in mucosal MPO activity between the Ws/Ws and control (+/+) rats (P = 0.46). (iv) The mucosal histamine levels in the colon were significantly reduced in the Ws/Ws rats compared with the control (+/+) rats (P < 0.05). (v) Significant positive correlations were observed between mucosal histamine levels and the degree of mucosal oedema (calculated as colonic wet weight/protein content) (r = 0.778, P < 0.01), and between histamine levels and the macroscopic damage (r = 0.623, P < 0.05), respectively. (vi) DSS induced a local recruitment of MMC in the colonic mucosa of Ws/Ws rats, and mucosal damage gradually increased in accordance with this MMC recruitment. These results indicate that MMC play an important role in the development of DSS colitis.

Animals↗
PubMed1998

Colonic carcinomas masquerading as Crohn's colitis.

When colonic carcinomas present with acute abdomen, the operating surgeon and the pathologist face a plethora of diagnostic and therapeutic problems. In this retrospective study of 92 cases of carcinoma colon, 4 presented with acute intestinal obstruction of which three had a turbulent post operative period and died. The resected colonic segment showed on gross examination cobblestone appearance characteristic of Crohn's disease but microscopically was ischemic with the stricture site showing features of an infiltrating poorly differentiated adenocarcinoma. We have made an attempt to study the various pathologic features and analyse their significance with reference to prognosis.

Adenocarcinoma↗
PubMed1982

Evaluation of techniques for chemical debridement of colonic mucosa.

Rectal mucosectomy may be technically difficult to perform on certain patients with severe ulcerative colitis involving the rectum, in whom a colectomy and endorectal ileal pull-through operation is planned. The present study evaluates the effectiveness of the following caustic agents in causing severe injury to the colonic mucosa of dogs after ten minutes of exposure, as determined by light and scanning electron microscopy: 1.0 normal sodium hydroxide; 0.5 normal sodium hydroxide; 1.25 per cent formalin solution, and silver nitrate sticks. The 1.0 normal sodium hydroxide solution caused injury to both mucosa and muscularis. The 0.5 normal sodium hydroxide produced mucosal injury without damage to the muscularis; the mucosa could be rubbed off with minimal bleeding. Although the mucosa exposed to 1.25 per cent formalin solution or to silver nitrate sticks showed varying degrees of injury, the remaining mucosa was not readily removed by rubbing. Repeat exposure of the mucosa to 0.5 normal sodium hydroxide three days after the first exposure made it easy to remove the mucosa by gentle rubbing but did not cause gross or microscopic injury to the muscularis. Chemical debridement of colonic or rectal mucosa may be a helpful adjunct when the mucosa cannot be removed readily by standard surgical dissection during endorectal pull-through operations.

Animals↗
PubMed1998

Infiltration of peroxidase-producing eosinophils into the lamina propria of patients with ulcerative colitis.

Little information is available to explain the pathogenesis of ulcerative colitis (UC). In this study, we focused on eosinophils in the lamina propria of the mucosa of patients with UC in the active phase. Biopsy specimens were taken from 17 patients with UC in the active phase, 17 in the inactive phase, and 20 control patients, and submitted for histochemical staining for peroxidase and chloroacetate esterase for microscopic examination. Both peroxidase-producing and chloroacetate esterase-producing cells in the lamina propria increased markedly in the active phase (8.3 +/- 3.1/0.01 mm2 and 6.6 +/- 2.7/0.01 mm2, respectively), compared with values in the inactive phase (0.8 +/- 0.6/0.01 mm2 and 1.3 +/- 0.6/0.01 mm2) or in the controls (1.3 +/- 0.8/0.01 mm2 and 1.3 +/- 0.4/0.01 mm2). Triple staining for peroxidase, chloroacetate esterase, and nonspecific esterase in the specimens revealed that the peroxidase-producing cells constituted a different population from that of neutrophils, macrophages/monocytes, or basophils. A monoclonal antibody specific for eosinophil peroxidase stained almost all infiltrated peroxidase-producing cells. These results indicated that eosinophils with strong peroxidase activity had infiltrated the lamina propria in UC, suggesting an allergic background and the involvement of released peroxidase in the mucosal damage characteristic of UC.

Carboxylic Ester Hydrolases↗
PubMed1986

Campylobacter colitis in ranch mink in Ontario.

Outbreaks of colitis, where Campylobacter jejuni and Campylobacter coli were the only pathogens isolated occurred in weanling mink (Mustella vision) on two commercial mink ranches in Ontario. Lesions were restricted to the proximal colon and were characterized by multiple 1 mm focal or 1 mm linear erosions/ulcers in the region 2 cm distal to the ileal-colonic junction. Histological changes included thickening of the colonic mucosa, inflammatory cell infiltrate in the lamina propria and submucosa, cellular debris and inflammatory exudate within cryptal lumens and multiple areas of mucosal erosion/ulceration. Four C. jejuni negative mink were challenged with 5.1 X 10(9) colony forming units of C. jejuni by oral inoculation. Three of four experimentally infected mink developed diarrhea by day 4 postinfection with lesions grossly and microscopically similar to mink in the naturally occurring outbreak. Examination of lesions by transmission electron microscope failed to show evidence of C. jejuni invasion of intestinal epithelium. Feeding uncooked slaughterhouse chicken offal was the likely source of C. jejuni in the naturally occurring outbreaks.

Animals↗
PubMedDate not supplied

Changes in the rectal mucosa induced by hypertonic enemas.

The aspect of the rectal mucosa after administration of hypertonic enemas is occasionally confused with the macroscopic appearance of quiescent ulcerative colitis. Criteria for a diagnosis of enema reaction were derived from a retrospective series and tested prospectively on 11 healthy volunteers. Photographs and biopsies were obtained before and after administration of a sodium phosphate hypertonic enema. Three observers evaluated blindly the "before" and "after" macroscopic and microscopic pictures, graded the features, and made an overall diagnosis. In random studies, two observers mistakenly classified a macroscopic picture, but all correct histologic diagnoses of "before" and "after" biopsies. In decreasing order of discriminating power, the following features of an enema reaction were found to be useful: separation and mucous depletion of the glands (no observer variation), increase in mucosal fragility in 91 per cent of cases (82--100 per cent), edema of the lamina propria in 88 per cent (73--100 per cent), straightening of the basal membrane in 82 per cent (73--91 per cent) and an increase in extruded mucus in 70 per cent (18--100 per cent). In 39 per cent of cases (36--45 per cent), erythrocytes appeared focally in the lamina propria. The effects of hypertonic enemas can be recognized on biopsy.

Adult↗
PubMed1971

Electron microscopy in Crohn's disease.

An electron microscopic study of Crohn's disease of the colon is presented. The positive findings that supplement those obtained by light microscopy are: a prominent nucleolus is more common in the lymphocytes of Crohn's disease than in normal lymphocytes or those found in cases of ulcerative colitis; lymphocytes are often observed close to macrophages and epithelioid cells; the epithelioid cells are metabolically active, and have vesicles which contain acid phosphatase but little visible debris; intramural bacteria were identified in six of the 11 specimens of colon with intact epithelia and minimal inflammatory changes. The possible significance of these findings for the pathogenesis of the disease is discussed.

Acid Phosphatase↗
PubMed1996

Apoptosis of crypt epithelial cells in ulcerative colitis.

In the colon of ulcerative colitis (UC) patients, apoptotic bodies have been recognized in routine histopathological preparations. To investigate the extent of the apoptosis, colonic biopsies were examined from involved and uninvolved areas of untreated active UC and from normal areas in patients with colonic polyps, utilizing various markers of apoptosis. The markers included DNA breaks detected by TUNEL, Fas (CD95/APO-1) and Fas ligand (Fas-L) localized by immunohistochemistry, electron microscopic features of apoptosis, and laddering of extracted DNA. Apoptosis marker positive cells were found mainly on the luminal epithelium of the normal colon and were present in active UC in crypts of involved and uninvolved areas of the colon, in addition to the luminal epithelium. The DNA extracted from active UC colon electrophoresed as a ladder. These findings suggest that the loss of epithelial cells in active UC occurs mainly by apoptosis in crypts of involved and adjacent uninvolved areas and that the Fas/Fas-L interaction is a mediator of the apoptosis.

Apoptosis↗
PubMed1993

MR imaging of ulcerative colitis.

High-resolution magnetic resonance imaging (MRI) was used to study 16 resected rectosigmoid specimens of patients treated with total colectomy for severe ulcerative colitis (UC). Six normal colon specimens were also studied as a control group. Moreover, a parallel study of the pelvis of 24 patients with a proven diagnosis of UC was performed with the same MR system. Both in vitro and in vivo MRI findings [thickening and signal intensity (SI)] of the mural layers were qualitatively evaluated by two radiologists and compared with gross and microscopic aspects. In vitro results showed that MRI was able to identify all layers of the colonic wall. In particular in UC specimens, MRI identified thickening and the peculiar abnormal hyperintensity of the mucosal and submucosal layers on spin-echo (SE) T1-weighted images. In vivo results confirmed the high-signal intensity of the mucosal and submucosal layers. These findings were not observed in the control group in which the superficial layers appeared low in intensity on SE T1 images. Our preliminary experience suggests that MRI should be considered a new imaging modality for detecting UC colonic wall changes.

Adult↗
PubMed1992

Microbic superinfection in relapse of inflammatory bowel disease.

To assess the association between symptomatic relapse of inflammatory bowel disease (IBD) and superinfection with enteropathogenic microorganisms, we determined prospectively the incidence of infections with enteropathogenic bacteria, protozoa, and helminths in patients with confirmed longstanding IBD. Sixty-four patients with IBD (49 with Crohn's disease [CD] and 15 with ulcerative colitis [UC]) were consecutively enrolled in the study when relapse occurred. Multiple biopsies for histological and microbiological investigations were taken from all patients who were evaluated by colonoscopy. Parallel stool specimens were investigated for the presence of enteropathogenic bacteria, protozoa, and helminths. In six patients, we detected Clostridium difficile or toxin B (five CD, one UC), in one patient Campylobacter jejuni (CD), and in another patient Salmonella typhimurium (UC). Enteropathogenic Escherichia coli were isolated from three patients. Investigation of biopsies for Mycobacteria, microscopic examination of stool samples for helminths, and immunofluorescence for chlamydia were negative in all patients. In summary, as we found enteropathogenic microorganisms so infrequently in patients with relapse of IBD, despite intensive microbiological screening by tissue sampling for detection of gut adherent bacteria, we believe that microorganisms play only a minor role in the exacerbation of IBD.

Adult↗
PubMed1976

Ulcerative colitus and Crohn's disease of the colon - a comparison of the long term postoperative courses.

Patients with colitis and ileocolitis of unknown etiology from two previously reported series have been combined and the follow-up studies have been extended to compare the long term postoperative courses of ulcerative colitis (UC) and Crohn's disease of the colon (CDC). The combined and updated series of 176 patients, 99% of whom could be traced, provided a mean postoperative follow-up period for UC of 14 years (5 to 31) and CDC of 13.1 years (5 to 36). There were highly significant associations between generally accepted clinical and distributional features of UC and CDC and microscopic findings generally regarded as reliable for each. However, because of spectrum of features was found in each entity, neither clinical and distributional nor microscopic features alone are sufficient for diagnosis in every case. There were no differences in gross or disease-related mortality in UC and CDC whatever the method of diagnosis. After anastomotic procedures in CDC a recurrence rate of 73% was found. After proctocolectomy the ileostomy revision rate (considering all types of those which required further excision of ileum) was higher in CDC than UC whether the diagnoses were based on microscopic, clinical, or combined criteria, but the differences reached statistical significance only in the comparison of "clinical UC", with "clinical CDC". Moreover, after the first 2 postoperative years, the risk of having an ileostomy revision in UC and CDC (combined criteria) per patient year follow-up was virtually identical and there were no cases of short bowel syndrome. Differences in the clinical courses of UC and CDC after colectomy and ileostomy are of degree and do not reflect the ultimate course or potential for rehabilitation. Decisions regarding surgical therapy should be made independent of the diagnosis of UC or CDC.

Colectomy↗