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PubMed2004

Pro-oxidant environment of the colon compared to the small intestine may contribute to greater cancer susceptibility.

The colon and small intestine have inherent differences (e.g. redox status) that may explain the variation in cancer occurrence at these two sites. This study examined basal and induced (oxidative challenge) reactive oxygen species (ROS) generation, antioxidant enzyme activity and oxidative DNA damage. Basal ROS and antioxidant enzyme activities in the colon were greater than in the small intestine. During oxidative stress, 8-oxo-deoxyguanosine (8-oxodG) DNA adducts in the colon exceeded levels in the small intestine concomitant with increased ROS. Thus the colon responds to oxidative stress less effectively than the small intestine, possibly contributing to increased cancer incidence at this site.

Animals↗
PubMed1982

An immunohistochemical investigation of vasoactive intestinal polypeptide in the colon of patients with Hirschsprung's disease.

The distribution of vasoactive intestinal polypeptide (VIP) in the colon of patients with Hirschsprung's disease was investigated by the peroxidase-antiperoxidase (PAP) immunohistochemical method. Three colonic segments, ganglionic, oligoganglionic and aganglionic, were stained by the unlabeled antibody enzyme method. VIP immunoreactive nerve cell bodies, nerve fibers and nerve endings were distributed throughout the ganglionic and oligoganglionic segments. In contrast, the aganglionic segment contained no VIP nerve endings and the number of fibers was reduced. These differences are thought to be a cause of constriction of the colon in Hirschsprung's disease and VIP neurons are therefore believed to participate in the relaxation of smooth muscle.

Child↗
PubMed1985

Electron microscopy of the intestine and rectum in acquired immunodeficiency syndrome.

To provide a better understanding of the morphologic changes that take place in the intestine and colon in acquired immunodeficiency syndrome (AIDS), electron microscopy was performed on intestinal or colonic biopsy specimens obtained from 6 patients with AIDS and from 2 patients with AIDS-related lymphadenopathy syndrome. Cryptosporidia were attached to the plasma membrane of epithelial cells in 2 patients and were noninvasive. An invasive protozoan organism identified as Microsporidia was found in 1 patient. Evidence for epithelial cell injury was limited. Unusually prominent secretory granules in colonic epithelial cells (a morphologic counterpart of secretion) was found in 2 patients. Tubuloreticular structures were observed in 7 patients. The structures were found in endothelial cells, lymphocytes, monocytes, intraepithelial lymphocytes, and free in the capillary lumen. Tube- and ring-shaped forms were observed in 2 patients, prominent intraepithelial mast cells in 4 patients, rectal spirochetosis in 1 patient, and pseudomembranous colitis in 1 patient with intestinal and systemic shigellosis. Vesicular rosettes, retroviruses, other viruses, and Mycobacterium avium-intracellulare were not observed. These observations expand our knowledge of morphologic changes in the colonic and intestinal mucosa in patients with AIDS. Tubuloreticular structures are so prominent, in contrast to our previous electron-microscopic observations in other disease and normal states of the intestine and colon, that their finding (though clearly nonspecific) may be a clue to the diagnosis of AIDS in an otherwise equivocal situation.

Acquired Immunodeficiency Syndrome↗
PubMed2006

Salmonella Typhimurium SPI-1 genes promote intestinal but not tonsillar colonization in pigs.

Salmonella Pathogenicity Island 1 (SPI-1) genes are indispensable for virulence of Salmonella Typhimurium in several animal species. The role of SPI-1 in the pathogenesis of Salmonella Typhimurium infections of pigs, however, is not well described. The interactions of a porcine Salmonella Typhimurium field strain and its isogenic mutants with disruptions in the SPI-1 genes hilA, sipA and sipB with porcine intestinal epithelial cells were characterized in vitro and in a ligated intestinal loop model in pigs. HilA and SipB were essential in the invasion of porcine intestinal epithelial cells in vitro. A sipA mutant was impaired for invasion using a polarized cell line, but fully invasive in a non-polarized cell line. All SPI-1 mutants induced a significant decrease in influx of neutrophils in the porcine intestinal loop model compared with the wild type strain. Pigs were orally inoculated with 10(8) colony forming units of both the wild type Salmonella Typhimurium strain and its isogenic sipB::kan mutant strain. The sipB mutant strain was significantly impaired to invade the intestinal, but not the tonsillar tissue, one day after inoculation and was unable to efficiently colonize the intestines and the GALT, but not the tonsils, 3 days after inoculation. This study shows that SPI-1 plays a crucial role in the invasion and colonization of the porcine gut and in the induction of influx of neutrophils towards the intestinal lumen, but not in the colonization of the tonsils.

Animals↗
PubMed1981

Reduced tissue content of vasoactive intestinal peptide in aganglionic colon of Hirschsprung's disease.

The colonic tissue content of immunoreactive vasoactive intestinal peptide was measured in four children with histologically proven Hirschsprung's disease. The concentration of vasoactive intestinal peptide was lower in the aganglionic bowel than in nearby normal bowel. Similar results have been described for another gastrointestinal peptide: substance P. Abnormalities of peptidergic control may contribute to the motility disorder of congenital aganglionic colon.

Child↗
PubMed1991

Study of colonization resistance for Enterobacteriaceae in man by experimental contamination and biotyping as well as the possible role of antibodies in the clearance of these bacteria from the intestines.

The colonization resistance (CR) of the digestive tract was determined in 10 healthy volunteers by oral contamination with a neomycin resistant Escherichia coli (NR-E. coli) strain and measurement of the faecal concentration of this strain during 14 days after the contamination. This 'gold standard' was compared with another parameter of CR; the determination of the mean number of different biotypes of Enterobacteriaceae isolated from four faecal samples per volunteer. Both measures are significantly correlated (P less than 0.01). The NR-E. coli strain could be cultured from faecal samples of 4/10 volunteers as long as 300 days after contamination. Serum antibody titres against endogenous E. coli strains and the NR-E. coli strain used for experimental oral contamination were measured by an indirect immunofluorescence (IIF) assay. The assay was read by a video camera connected to an image processing system. The 95% confidence limits of antibody titres (log2) against endogenous E. coli strains ranged between less than 3 and 7.1 for IgA, between less than 3 and 8.7 for IgG and between less than 3 and 7.4 for IgM. Antibody titres against the NR-E. coli4 strain were within this (normal) range. The serum antibody titres against the NR-E. coli strain increased slowly after oral contamination, especially IgG and IgM. Little increase in IgA titres could be observed. An increase of serum antibody titres did not correlate with the elimination of the oral contaminant from the intestines. Therefore, we conclude that the CR is not IgG nor IgM antibody mediated.

Adult↗
PubMed1995

Phenotypic characterization of intestinal Escherichia coli of pigs during suckling, postweaning, and fattening periods.

A highly discriminatory and standardized biochemical fingerprinting method was used to monitor the persistence and colonization of intestinal Escherichia coli isolated from the feces of four sows and their litters (four piglets from each) during the suckling, postweaning, and fattening periods. Altogether, 195 fecal samples were collected and 1,827 E. coli strains were tested (mean number of isolates tested per fecal sample per pig, 9.5). Strains were divided into similarity groups on the basis of their biochemical phenotypes (BPTs). The diversity of E. coli strains in each sample was measured with Simpson's index of diversity, and similarity between E. coli floras of piglets was calculated with a population similarity index. Each fecal sample contained several BPTs of E. coli, some of which dominated that population. The intestinal colonization of piglets consisted of successive waves of different E. coli BPTs, the tenure of which varied from a few days to 2 weeks. Most of these BPTs disappeared in the succeeding samples and were not recovered again from the same piglets. On the other hand, some E. coli strains which colonized piglets early during the suckling period persisted for a long period and were referred to as resident BPTs. Each piglet carried more than one resident BPT (mean of 2.4 BPTs per pig), some of which were also found in other piglets.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Immunohistochemical localization of insulin-degrading enzyme along the rat intestine, in the human colon adenocarcinoma cell line (Caco-2), and in human ileum.

Insulin-degrading enzyme (IDE) has been implicated in the intracellular degradation of insulin in insulin target cells. Knowledge of the existence of this enzyme in the intestine will be beneficial to the achievement of clinical oral efficacy of insulin. A comparative study was conducted with rat intestine, human colon adenocarcinoma (Caco-2) cells, and human ileum. Confocal microscopy analysis using the anti-IDE antibody showed that IDE was localized in the mucosal cells of rat and human intestines, as well as in Caco-2 cells. Immunostaining of this enzyme was homogeneous throughout the cell excluding nucleus, indicating a typical cytosolic distribution in rat and human enterocytes and in Caco-2 cells.

Adenocarcinoma↗
PubMed1995

Intercellular signals downstream of endothelin receptor-B mediate colonization of the large intestine by enteric neuroblasts.

Mice homozygous for the piebald lethal (sl) mutation, which have a complete deletion of endothelin receptor-B, fail to form ganglion cells in the distal large intestine and are nearly devoid of cutaneous melanocytes. These phenotypic features stem from incomplete colonization of the hindgut and skin by neural crest-derived neuroblasts and melanoblasts, respectively. We have used expression of a transgene, dopamine-beta-hydroxylase-nlacZ, to study colonization of the enteric nervous system in sl/sl embryos and sl/sl <--> wild-type chimeric mice. Enteric neuroblasts derived from the vagal neural crest colonize the developing foregut, midgut and distal small intestine of sl/sl embryos in a cranial-to-caudal manner indistinguishable from sl/+ or +/+ embryos. However, colonization of the large intestine is retarded and the distal large intestine is never colonized, a developmental defect identical to that observed in lethal spotted (endothelin-3 deficient) embryos. The coat pigmentation and relative distributions of mutant and wild-type ganglion cells in sl/sl <--> wild-type chimeras indicate that the defect associated with endothelin receptor-B gene deletion is not strictly neuroblast autonomous (independent of environmental factors). Instead, intercellular interactions downstream of the endothelin receptor-B mediate complete colonization of the skin and gut by neural crest cells.

Animals↗
PubMed1978

Multiple immunoreactive forms of vasoactive intestinal peptide in human colonic mucosa.

Extracts of human colon mucosa and muscle were fractionated by gel filtration and ion exchange chromatography and molecular forms of vasoactive intestinal peptide (VIP) estimated by radioimmunoassay. Total concentrations of immunoreactive VIP in mucosa were 237.1 +/- 53.9 and 119 +/- 26.0 pmoles per g in muscle. In muscle, over 90% of the immunoreactivity was accounted for by a single component indistinguishable from porcine VIP by gel filtration and ion exchange chromatography. In contrast, mucosa contained four components with VIP-like immunoreactivity. One of these had the chromatographic properties of porcine VIP; the others were less positively charged. Two of the new VIP-like components had gel filtration properties similar to those of VIP and are, therefore, probably of similar size to the porcine octacosapeptide, and the remaining component emerged later on Sephadex and is, therefore, probably a smaller peptide. Immunoreactive VIP in muscle extracts is believed to originate from nerve fibers, and this form of VIP is likely to be identical to the previously characterized form of VIP. However, immunoreactive VIP in mucosal extracts may originate either from endocrine cells or nerve fibers. The possibility arises, then, that there are different immunoreactive forms of VIP in nerves and endocrine cells.

Animals↗
PubMed1987

Intramucosal cysts in gastric mucosa adjacent to carcinoma and peptic ulcer: a histochemical study.

Histochemical characteristics and the distribution of gastric intramucosal cysts were studied in 50 cancerous and 51 benign gastrectomy specimens. The frequency of such cysts was significantly higher in stomachs with carcinoma (70%) than in stomachs with peptic ulcer (43%) (P less than 0.01). Intramucosal cysts were classified into gastric type, small intestinal type, colonic type and non-mucous type. There were significant differences in the constituent ratios of the four types of cyst between gastric carcinoma and gastric ulcer (P less than 0.01), as well as between intestinal type and diffuse type cancer (P less than 0.001). The present results reveal a close relationship between intramucosal cysts and gastric carcinoma. Cysts of small intestinal, colonic and non-mucous types were associated with intestinal type cancer while cysts of gastric type were related to diffuse type cancer of the stomach.

Cysts↗
PubMed1987

The maximal activity of phosphate-dependent glutaminase and glutamine metabolism in the colon and the small intestine of streptozotocin-diabetic rats.

The effects of short- and long-term diabetes on the maximal activities of phosphate-dependent glutaminase and glutamine metabolism were studied in the colon and the small intestine of streptozotocin-diabetic rats. The maximal activity of colonic phosphate-dependent glutaminase was decreased [44% in mucosal scrapings (p less than 0.01); 29% in whole colon (p less than 0.001)] or unchanged in short- or long-term diabetes respectively. That of the small intestine was increased in both short- (110%) and long-term (200%-500%) diabetes; insulin treatment corrected this increase. Acute insulin-deficiency (using anti-insulin serum) resulted in the increase (18%, p less than 0.05) of the activity of only intestinal glutaminase. Chemically-induced acidosis and alkalosis decreased (46%, p less than 0.001) and increased (24%, p less than 0.001), respectively, the activity of intestinal glutaminase, but had no effect on the colonic enzyme. Changes in glutaminase of the enlarged colon and small intestine were only detectable when activities were measured in whole organ. Arteriovenous-difference measurements showed diminished metabolism of plasma glutamine by the gut which correlated with the duration of the state of diabetes, and was accompanied by enhanced release by skeletal muscle and increased uptake by both kidney and liver. It is concluded that insulin is directly or indirectly involved in the regulation of glutamine metabolism of the gut.

Acidosis↗
PubMed2004

Colonization of the neonatal rat intestinal tract from environmental exposure to the anaerobic bacterium Oxalobacter formigenes.

Oxalobacter formigenes, an anaerobic bacterium that inhabits the mammalian gastrointestinal tract, has an important symbiotic relationship with its vertebrate hosts by regulating oxalic acid homeostasis. Epidemiological studies of O. formigenes colonization in man have shown that colonization occurs in young children, that every child can become colonized naturally, that >20% lose colonization during adolescence or as adults and that stable colonization can be disrupted by antibiotic use or changes in diet, greatly affecting subsequent health. As O. formigenes is a fastidious anaerobe that seldom re-colonizes adults, the question arises as to how initial colonization occurs. To investigate this question, non-colonized female laboratory rats were placed on diets high in oxalate and were colonized by oesophageal gavage with O. formigenes either before or after being impregnated. Faecal specimens from their offspring were tested for the presence of O. formigenes. Although the bacterium was first detected in a few neonates as early as 7 days post-partum, colonization of all the offspring did not occur until after weaning. In each case, the offspring were colonized with the bacterial strain carried by their mothers. To determine whether O. formigenes colonization occurs vertically or horizontally, newborn rats were placed with foster mothers that were either non-colonized or colonized with an O. formigenes strain different from that of their natural mothers. Colonization occurred temporally in a manner similar to natural colonization but all offspring became colonized only with the O. formigenes strain of the foster mothers. These data indicate that intestinal colonization occurs horizontally, but does not answer the question of how O. formigenes survives the aerobic environment in order to be transmitted.

Animals↗
PubMed1982

The prevalence and significance of gastritis in patients with lower intestinal irritable bowel (irritable colon) syndrome.

Histological gastritis was present in nearly two-thirds of consecutive patients with lower intestinal irritable bowel (irritable colon) syndrome. The presence of gastritis had no relationship to upper intestinal symptoms; we believe that upper intestinal symptoms in these patients are therefore unlikely to be due to coexistent gastritis. Abnormal pyloroduodenal motility with consequent abnormal bile reflux or clearance may account for gastritis in patients with irritable colon. This study, admittedly uncontrolled, provides further indirect evidence to support the concept of a widespread neuromuscular abnormality throughout the gastrointestinal tract in irritable bowel syndrome patients who have predominantly colonic symptoms.

Adolescent↗
PubMed1999

Isoforms of the human PDZ-73 protein exhibit differential tissue expression.

Patients with renal and colon cancer frequently develop IgG autoantibodies toward the NY-CO-38/PDZ-73 antigen, a protein of 652 amino acids (73 kDa) which contains three copies of the PDZ protein-protein interaction domain. The gene encoding PDZ-73 mapped to chromosome 11p15.4-p15.1. Additional tissue-specific isoforms were identified: PDZ-45, which lacks the third PDZ domain and the putative PEST protein degradation motif, is expressed in kidney, colon, small intestine, brain and testis; PDZ-54 and PDZ-59, which also lack the third PDZ domains, have unique carboxyl terminal amino acids and are expressed in brain, kidney, bladder, colon cancer and renal cancer; and a putative PDZ-37 isoform, containing only the third PDZ domain, that is expressed in the central nervous system. Immunohistochemical staining with anti-PDZ 73 monoclonal antibodies showed strong cytoplasmic reactivity in epithelial cells of the small intestine, colon and kidney tubules, with a prominent apical staining pattern in cells of the small intestine. The reactivity pattern of the antibodies with various tissues correlated with the mRNA expression pattern of the PDZ-45 isoform. The existence of multiple PDZ-73 isoforms with variations in tissue distribution, PDZ domains, protein degradation sequences and carboxyl terminal structure indicate that these isoforms have distinct tissue-specific functions.

Adaptor Proteins, Signal Transducing↗
PubMed1984

Immunohistological evidence, obtained with monoclonal antibodies, of small intestinal brush border hydrolases in human colon cancers and foetal colons.

The expression of small intestinal hydrolases associated with the enterocyte brush border membrane was studied in human colon cancers and foetal colons, by means of monoclonal antibodies against human small intestinal sucrase-isomaltase (SI), maltase-glucoamylase (MGA), lactase (L), aminopeptidase N (APN), and dipeptidylpeptidase IV (DPP-IV). The enzymes were visualized by indirect immunofluorescence on cryostat sections of tumors developed in nude mice with 6 human colon carcinoma cell lines (HT-29, Caco-2, SW-480, HRT-18, HCT-8R, and Co-115), of 27 primary colorectal carcinomas from patients, and of human foetal (16 to 20 weeks of gestation) and normal adult small intestines and colons. All 5 monoclonals bound to the brush border of the adult small intestine, but not to that of the adult colon mucosa. Antibodies against SI, APN and DPP-IV also bound to the brush border of the foetal colons, to apical borders in HT-29 and Caco-2 tumors in nude mice, and to brush border-like structures in 7/27 tumors from patients. No binding was observed for MGA and L in either tumors or foetal colons. Binding of anti-SI antibodies to the brush border of the juxta-tumoral mucosal epithelium was observed in 9/11 samples tested. These data indicate that some colon tumors exhibit a typical pattern of enterocytic differentiation which is of foetal type and which involves at least 3 brush border membrane hydrolases. Monoclonal antibodies to small intestinal hydrolases may, therefore, be important tools for identification and characterization of some differentiated colonic tumors.

Antibodies, Monoclonal↗
PubMed1995

[Combined parenteral and oral immunization against enterotoxigenic Escherichia coli diarrhea in weaned piglets].

Experiments were focused on diarrhea prevention in weaned piglets caused by enterotoxigenic strains of Escherichia coli (ETEC) with colonizing factor 8813. An immunization procedure consisted of intramuscular application of ETEC strain bacterin a day before weaning and a peroral administration of a live culture of nontoxic E. coli strain with the same colonizing factor on the day of weaning. In an experiment on the litter of 10 piglets (six were immunized, four were controls), their intestines were colonized by the nontoxic E. coli strain for 4-7 days (Fig. 1). The challenge peroral infection by virulent ETEC strain demonstrated the protection of immunized piglets from the disease as well as from intestinal colonization by the administered ETEC strain. The same immunization procedure was tested on three pig farms with enzootic occurrence of diarrheas in weaned piglets. On these farms, besides ETEC strain with colonizing factor 8813 (F18) ETEC strains with other colonizing factors (K88, F not specified) were found out in the weanlings - Tab. I. Immunization effect was evaluated according to the rate of mortality of immunized and nonimmunized piglets within a fortnight after weaning. Out of 222 immunized piglets on S farm (Tab. II), 25 piglets died (11.3%), out of 232 nonimmunized animals it was 39 that died (16.8%). As for T farm (Tab. III), 22 piglets (8.6%) died out of 255 immunized animals while 71 out of control 274 piglets died (25.7%). A total of 3,692 were immunized on V farm (Tab. IV). Ninety-four animals died among them (2.5%). Mortality rate in the control group of 6,301 animals was 523 piglets (8.3%).

Administration, Oral↗
PubMed2000

Edema disease.

Edema disease is a common cause of illness and death loss in pigs during the first 2 weeks after weaning. The disease is an enterotoxemia caused by strains of E. coli that colonize the small intestine and produce Stx2e. Bacterial colonization is mediated by F18ab fimbriae. Susceptibility to disease is determined by presence of receptors for these fimbriae on small intestinal epithelial cells and is inherited as a dominant trait. Clinical signs and lesions are largely the result of Stx2e, which causes necrosis of endothelial and smooth muscle cells in small arteries and arterioles. Vascular damage in the brain stem with resultant infarction and malacia is the main cause of death in affected pigs. Studies conducted by veterinary researchers in the 1950s and 1960s identified the cause of the disease and provided future scientists with hypotheses to test regarding the pathogenesis. In the last two decades, studies using molecular-based techniques have allowed for the definitive identification of bacterial virulence factors that mediate intestinal colonization and vascular damage, that is, F18ab fimbriae and Stx2e. Identification of these virulence factors has provided a basis for current and future development of effective preventative measures, for example, vaccines.

Animals↗