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PubMed2005

[Experimental infection of mice with Blastocystis hominis].

OBJECTIVE: To seek a better pathway and proper number of parasites for Blastocystis hominis (B.h) infection in normal and immunocompromised ICR mice. METHODS: (1) 10(4), 10(5) and 10(6) B.h, cultured in RPMI 1640 medium from 3 generations were used to infect mice through oral and rectum; (2) 10(6) B.h were used to infect immunocompromised mice through rectum. The reproduction of B.h in gastrointestinal tract and the pathologic changes in the tissues were observed. RESULTS: Mice were infected by B.h through either oral or rectum. The infected immunocompromised mice showed slow locomotion, depressed, lethargy, and descended body weight. Some infected mice discharged mucus feces, a few of them died during the experiment. Parasites were found in the whole gastrointestinal tract. Severe edema, hyperemia and congestion were observed in the tissues of jejunum, ileum, cecum and colon. The epithelia of small intestine and colonic mucous membrane showed exfoliation, inflammatory cell infiltration in submucosa, and structural changes in glands. CONCLUSION: Mice were more susceptible to Blastocystis hominis infection through rectum than orally. The parasites can be found in the whole gastrointestinal tract of mice, and can breed rapidly and cause significant pathological change in the gastrointestinal mucosa in immunocompromised mice.

Animals↗
PubMed1999

Intestinal haemorrhage associated with colonic vascular ectasia (angiodysplasia) in a dog.

An eight-year-old, sexually intact, male, 37 kg crossbred dog was referred for investigation of two acute episodes of intestinal bleeding and severe anaemia within a five-month period. There was no evidence of coagulopathy or underlying systemic disease. Technetium-labelled red blood cell scintigraphy suggested the colon as the site of bleeding. Colonoscopy identified a focal area of dilated and tortuous mucosal blood vessels. Histopathology of the resected colon revealed vascular ectasia (angiodysplasia). At nine months post-resection, the dog remained healthy and free of any overt intestinal haemorrhage.

Anemia↗
PubMed1991

Effect of endothelin-1 and vasoactive intestinal contractor on blood flow and output of vasoactive intestinal polypeptide in the feline colon.

Injection of the structurally related peptides, endothelin-1 and vasoactive intestinal contractor (VIC), into a branch of the superior mesenteric artery in anesthetized cats caused dose-dependent reductions in blood flow in the portal vein and inferior mesenteric artery. The maximum effect occurred after 1 minute and was more prolonged in the portal vein. The effects of the two peptides were not significantly different. The colonic output of vasoactive intestinal polypeptide (VIP) into portal venous blood was decreased significantly by endothelin-1 and VIC, returning to baseline more rapidly than blood flow. When norepinephrine was injected to produce comparable reductions in blood flow, the output of VIP into portal venous blood was not altered significantly. These results suggest that inhibition of output of the vasodilator VIP contributes to the vasoconstrictor effects of endothelin-1 and VIC in the feline colonic vascular bed.

Animals↗
PubMed1980

The effect of dietary fibre on bile acid metabolism in rats.

1. Forty-eight male rats were fed sequentially for 14 d periods on diets containing different fibre contents. 2. One of the high-fibre diets was a commercial pelleted diet. The other was a low-fibre diet supplemented with 200 g wheat bran/kg. 3. At the end of each feeding period eight rats were killed. Liver microsomal cholesterol 7 alpha-hydroxylase (EC 1.14.1.-) activity and bile acid content of small intestine and colon were determined. 4. The different diets did not significantly alter the total intestinal bile acids, but affected the distribution and qualitative pattern in the colon and small intestine. 5. On the high-fibre diets deoxycholate, and hyodeoxycholate tended to be increased. 6. On the low-fibre diets the alpha, beta- and omega-muricholic acids tended to be increased. 7. Liver microsomal cholesterol 7 alpha-hydroxylase activity was lower in rats on the low-fibre and bran-supplemented low-fibre diets compared with that in rats fed on the commercial pelleted diet.

Animals↗
PubMed2005

An exceptional combined malformation: duplication of the urinary and intestinal tracts and the vulva (04-80CR).

The authors reported the surgical treatment of a 2-year-old girl with complete duplication of the kidney, ureter, bladder, urethra, and the vulva, associated with intestinal duplication and complete duplication of the appendix and colon. Congenital intestinal malrotation also concurred. After a series of preoperative examinations, exploratory operation including reduction of intestinal malrotation, fusion of bladder and colon, obliteration of the duplicated urethra, resection of the intestinal and appendiceal duplications, and cosmetic repair of the vulva was performed. Incontinence of urine and stool disappeared, and she had been followed up for 10 months until this report. Repeat voiding cystourethrography performed recently demonstrated a fused bladder and the disappearance of the duplicated urethra.

Abnormalities, Multiple↗
PubMed1996

CAM 17.1--a new diagnostic marker in pancreatic cancer.

CAM 17.1-Ab is a recently described monoclonal antibody that detects a mucus glycoprotein with high specificity for intestinal mucus, particularly in the colon, small intestine, biliary tract and pancreas. We investigated the expression and release of CAM 17.1 in pancreatic carcinoma cell lines and tissue specimens of normal pancreas, chronic pancreatitis and pancreatic cancer. CAM 17.1 was weakly expressed on normal ductal cells and chronic pancreatitis, whereas it was overexpressed in pancreatic cancer. Serum analysis using a new enzyme-linked antibody sandwich assay (CAM 17.1/WGA) of patients with chronic pancreatitis, pancreatic cancer or other gastrointestinal cancer and of healthy blood donors revealed a high sensitivity (67%) and excellent specificity (90%) of CAM 17.1/WGA assay in pancreatic cancer. In comparison with the tumour marker CA19-9, the sensitivity of the CAM 17.1/WGA assay was similar to the sensitivity of CA 19-9 (67% and 76%, P = 0.22), whereas the specificity of CAM 17.1/WGA assay was higher than in CA 19-9 (90% compared with 78% in chronic pancreatitis, P > 0.05).

Adult↗
PubMed1992

Movement along actin filaments of the perijunctional area and de novo polymerization of cellular actin are required for Shigella flexneri colonization of epithelial Caco-2 cell monolayers.

Shigella flexneri invades eucaryotic cells and grows in the cytoplasm. Lysis of the phagosomal membrane is a prerequisite for both intracellular multiplication and movement of the bacteria that gain direct access to the host cell actin. In HeLa cells, bacteria generate their own movement essentially by inducing actin polymerization. Polymerization of actin enables them to move rapidly and randomly in the cytoplasm and to spread from one cell to another through protrusions of the host cell membrane. This movement was designated the Ics phenotype. In contrast, in chicken embryo fibroblasts, bacteria move along actin filaments in a very organized manner, following the cytoskeletal architecture; this movement was designated the Olm phenotype. Bacterial movement is a major virulence factor in that it is necessary for efficient colonization of the intestinal epithelium of infected macaque monkeys. Further characterization of the cellular events that lead to colonization of the colonic intestinal epithelium was needed. In order to characterize the movement in vitro in a cell assay system more closely related to the intestinal epithelium, we used human colonic epithelial Caco-2 cells. The movement of bacteria as observed by using immunofluorescence and confocal microscopy appeared to result from the expression of both the Olm and Ics phenotypes. The former allowed colonization of cells along the actin filament ring of the perijunctional area. The latter promoted passage from one cell to adjacent cells. This in vitro pattern of movement and multiplication gives S. flexneri, once it has entered an epithelial cell, the unique capacity to spread through the entire epithelial layer without having further contact with the extracellular compartment.

Actin Cytoskeleton↗
PubMed1993

Variation in rotavirus virulence: a comparison of pathogenesis in calves between two rotaviruses of different virulence.

Variation in virulence between two bovine rotaviruses was investigated using ten female and ten male 10-day-old gnotobiotic calves of five breeds or cross breeds that were inoculated with a virulent strain or a strain of low virulence. Similar numbers of infectious viral particles were detected in feces of calves inoculated with either virus, but diarrhea, xylose malabsorption, and reduction of villus height occurred only after inoculation with virulent virus. The mean percentage of the area of the villus epithelium per villus immunostained for rotavirus antigen was eight times greater in calves inoculated with virulent virus, and the mean percentage of villi on which immunostained enterocytes were detected was twice as large in calves inoculated with virulent virus than in calves inoculated with the virus of low virulence. Mean crypt death and mean crypt cell production rates were increased after inoculation with either virus. Virulence was associated with extensive spread of infection through the small intestine, preferential colonization of the proximal small intestine, and marked damage to enterocytes and villi. The virus of low virulence infected the proximal small intestine poorly, and although it infected more enterocytes in the mid and distal small intestine and replicated in them, causing cytopathic effects, it did not damage intestinal structure and affect function.

Animals↗
PubMed1988

[Management of short bowel syndrome in infants--experience of adjunctive surgical therapy in three cases].

During the past nine years period, we managed 7 cases with short bowel syndrome resulting from massive intestinal resection in the neonatal period. Six children, aged 2 to 8 years are alive, and one died from cardiomyopathy caused by selenium deficiency at the age of one year. The carbohydrate-free milk was used for initial enteral nutrition, and the result was encouraging in 4 cases. In 3 cases in which residual small bowel varied between 6.5 to 18 cm, the enteral feeding was not incapable. These cases underwent adjunctive surgical therapy. Tailoring jejunoplasty was performed in the first case, and bowel lengthening in the second case. In both cases enteral nutrition was advanced postoperatively. The third patient who had rapid intestinal transit time underwent isoperistaltic colon interposition. Intestinal transit time was increased and enteral nutrition was advanced gradually.

Child↗
PubMed1994

Xanomeline: a novel muscarinic receptor agonist with functional selectivity for M1 receptors.

Xanomeline [3(3-hexyloxy-1,2,5-thiadiazol-4-yl)-1,2,5,6-tetrahydro-1- methylpyridine] has been evaluated as a muscarinic receptor agonist. In vitro, xanomeline had high affinity for muscarinic receptors in brain homogenates, but had substantially less or no affinity for a number of other neurotransmitter receptors and uptake sites. In cells stably expressing genetic m1 receptors, xanomeline increased phospholipid hydrolysis in CHO, BHK and A9 L cells to 100, 72 and 55% of the nonselective agonist carbachol. In isolated tissues, xanomeline had high affinity for M1 receptors in the rabbit vas deferens (IC50 = 0.006 nM), low affinity for M2 receptors in guinea pig atria (EC50 = 3 microM), was a weak partial agonist in guinea pig ileum and was neither an agonist nor antagonist in guinea pig bladder. In vivo, xanomeline increased striatal levels of dopamine metabolites, presumably by acting at M1 heteroreceptors on dopamine neurons to increase dopamine release. In contrast, xanomeline had only a relatively small effect on acetylcholine levels in brain, indicating that it is devoid of actions at muscarinic autoreceptors. In the gastrointestinal tract, xanomeline inhibited small intestinal and colonic motility, but increased small intestinal transmural potential difference. In contrast to the nonselective muscarinic agonist oxotremorine, xanomeline did not produce salivation, tremor nor hypothermia; it did, however, increase heart rate. The present data are consistent with the interpretation that xanomeline is a novel muscarinic receptor agonist with functional selectivity for M1 muscarinic receptors both in vitro and in vivo.

Animals↗
PubMed2000

Chemopreventive effects of dietary folate on intestinal polyps in Apc+/-Msh2-/- mice.

Epidemiological and animal studies (reviewed in Y. I. Kim, J. Nutr. Biochemistry, 10: 66-88, 1999; J. B. Mason and T. Levesque, Oncology, 10: 1727-1743, 1996) suggest that dietary folate intake is inversely related to the risk of colorectal cancer. However, the optimal timing of folate intervention and mechanisms by which folate modulates colorectal carcinogenesis have not been clearly established. A recently developed murine model of intestinal tumorigenesis, which carries a heterozygous mutation in the Apc gene and a null mutation in the Msh2 gene (Apc+/-Msh2-/-), was used to determine the effect of dietary folate on intestinal tumorigenesis. Apc+/- Msh2-/- mice were randomized to receive either 0 or 8 mg of folate/kg diet starting at either 3 or 6 weeks of age. The 3- and 6-week diet starts represent intervention before and after the establishment of neoplastic foci, respectively. At 11 weeks of age, mice were killed, and the small intestines and colons were analyzed for adenomas and aberrant crypt foci (ACF). Serum folate concentrations were determined by a standard microbiological assay. Genomic DNA methylation was assessed by in vitro [3H]methyl incorporation into hepatic DNA and by a methyl-sensitive restriction digestion method. Microsatellite instability was determined in matched normal and polyp DNA from the small intestine and colon at 5 loci. Serum folate concentrations accurately reflected dietary folate levels (P < 0.005). Folate supplementation, started before the establishment of neoplastic foci, significantly decreased the number of small intestinal adenomas (by 2.7-fold; P = 0.004) and colonic ACF (by 2.8-fold; P = 0.028) and colonic adenomas (by 2.8-fold; P = 0.1) compared with a moderate degree of folate deficiency. In contrast, a moderately folate-deficient diet, started after the establishment of neoplastic foci, significantly reduced the number of small intestinal adenomas (by 4.2-fold; P = 0.001) but had no effect on colonic ACF and adenomas compared with folate supplementation. Genomic DNA methylation and microsatellite instability do not seem to play a major role in folate-modulated intestinal and colonic tumorigenesis in this model. In conclusion, in this murine model, dietary folate supplementation significantly protects against small intestinal and colorectal tumorigenesis if it is provided before the establishment of neoplastic foci However, if it is provided after the establishment of neoplastic foci, dietary folate seems to have an opposite effect. These data suggest that the timing of folate intervention is critical in providing an effective and safe chemopreventive effect on intestinal tumorigenesis. Notwithstanding the limitations associated with this model, our data suggest that the optimal timing of folate intervention must be established before folate supplementation can be used as a safe chemopreventive agent against colorectal cancer.

Adenoma↗
PubMed1995

Adhesion of different bifidobacteria strains to human enterocyte-like Caco-2 cells and comparison with in vivo study.

The validity of the in vitro adhesion tests performed with cultured cell lines, was determined in this study by comparison with results obtained in vivo, in a previous study. To make this experiment the in vitro adhesion tests were performed during a long period by utilization of an appropriate medium, to determine the capacity of the adhered strain to colonize the intestinal tract. It was demonstrated that the ability of the strain to adhere and colonize the intestinal cell in vivo or the cultured intestinal cells in intro was similar.

Bacterial Adhesion↗
PubMed1998

Partial intestinal obstruction due to colonic adenocarcinoma in a cat.

An abdominal mass was palpated in a 14-year-old, spayed female cat with unresolving diarrhea and decreased appetite. A stricture of the ascending colon was confirmed radiographically, identified upon laparotomy, and resected. Colonic adenocarcinoma with infiltration into lymphatics was diagnosed histologically. Eight months postoperatively, the subject was clinically normal.

Animals↗
PubMed1989

[Early administration of antibiotic susceptible strain of Escherichia coli in the intestine of the premature infant].

An antibiotic-susceptible, innocuous Escherichia coli strain of human origin was administered to premature infants in order to protect them from nosocomial colonization by antibiotic-resistant enteric organisms. The strain was given to 16 untreated patients in the first six hours of life, and to 11 patients treated with antibiotics in the first six hours after cessation of treatment. The strain was able to colonize the intestinal tracts of all treated infants and 14/16 untreated infants. Colonization of these patients by antibiotic-resistant enteric organisms was compared with results obtained in a control group of 15 unadministered and untreated infants. A significant difference was recorded in the first ten days after administration. Our results show that previous antibiotic treatments did not impair intestinal colonization by an antibiotic-susceptible strain, and demonstrate the in vivo antagonistic abilities of the administered strain. Such antagonistic strains might thus be used for control of nosocomial infections of intestinal origin due to antibiotic-resistant enteric organisms.

Cross Infection↗
PubMed1991

Comparative study of colonizing and noncolonizing Campylobacter jejuni.

Campylobacter jejuni A74/O and A74/C are congenic strains. An oral dose of 10(5) organisms of strain A74/C colonizes chicken intestines. Strain A74/O, from which A74/C is derived, does not colonize the chicken intestines with an oral dose of 10(5) organisms. In this study, the congenic bacteria were compared to identify possible colonization mechanisms. Differences were not observed in plasmid content or by HindIII, Pst I, Acc I, HincII, Ava I, Ava II, Xba I, and BamHI restriction enzyme digestion of total DNA. Transmission electron microscopy of negatively stained samples revealed no differences between the strains. Sections of cecal tissue from nonfed day-of-hatch chicks were cultured with each strain for 2 hours and then examined by light and electron microscopy. Both strains caused necrosis of villus epithelial cells. Immunofluorescent or silver staining revealed strain A74/C located deep in numerous epithelial crypts, but strain A74/O only was present in one sample mixed with sloughed necrotic cells. Similarly, organisms were detected by transmission electron microscopy deep in crypts in tissues cultured with A74/C, but not A74/O. Cells of A74/C detected in crypts did not appear to associate with epithelial cells. The strains did not differ in chemotactic behavior to mucin or fucose.

Animals↗
PubMed1981

Role of prostaglandins in the regulation of intestinal electrolyte transport.

The E prostaglandins (and to a lesser extent PGE2 alpha) stimulate active electrolyte secretion in mammalian small intestine and colon. They do so by stimulating intestinal mucosal adenylate cyclase and thereby increasing cAMP concentration. The diarrheagenic action of the prostaglandins is seen as a side effect of their therapeutic use, in certain hormone-secreting tumors, and in inflammatory lesions of the bowel in which leukocyte infiltrates are the probable sources of prostaglandin excess. Prostaglandins are also normally synthesized by intestinal epithelial cells and appear to play an important role in the physiologic regulation of intestinal fluid transport. In recent in vitro studies, we have shown that addition of arachidonic acid (K 1/2 congruent to 10(-6) M) also stimulates secretion, cAMP accumulation, and PGE2 production in rabbit ileal mucosa. In the continued presence of arachidonate, tachyphylaxis develops: both secretory and cAMP responses have a half-life of about twenty minutes and subsequent additions of arachidonate produce little or no further response. In contrast, PGE2 production continues undiminished. Similar tachyphylaxis develops when PGE2 itself is added. Resensitization following removal of PGE2 is rapid, 50% of the initial sensitivity being restored in 6-7 min. Prostaglandin desensitization has been noted in other cell systems and appears to be exerted on adenylate cyclase.

Adenylyl Cyclases↗
PubMed2001

Hypothesis: inappropriate colonization of the premature intestine can cause neonatal necrotizing enterocolitis.

Neonatal necrotizing enterocolitis (NEC) is a major cause of morbidity in preterm infants. We hypothesize that the intestinal injury in this disease is a consequence of synergy among three of the major risk factors for NEC: prematurity, enteral feeding, and bacterial colonization. Together these factors result in an exaggerated inflammatory response, leading to ischemic bowel necrosis. Human milk may decrease the incidence of NEC by decreasing pathogenic bacterial colonization, promoting growth of nonpathogenic flora, promoting maturation of the intestinal barrier, and ameliorating the proinflammatory response.

Digestive System↗