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PubMedDate not supplied

Regional differences in attachment of enteroadherent Escherichia coli strain RDEC-1 to rabbit intestine: luminal colonization but lack of mucosal adherence in jejunal self-filling blind loops.

RDEC-1 (serotype 015:NM) is an enteropathogenic Escherichia coli that adheres to mucosal epithelial cells in the ileum, cecum, and colon, but not in the jejunum, of rabbits during diarrheal illness. As RDEC-1 can adhere to jejunal brush borders in vitro, rapid distal clearing of the enteropathogen from the upper gastrointestinal tract may explain the absence of in vivo adherence of RDEC-1 to rabbit jejunum. To test this hypothesis, self-filling blind loops (SFBL) were created in the jejunum of rabbits that were then inoculated with RDEC-1 to determine if stasis would promote increased luminal colonization and increased mucosal attachment of RDEC-1 in the proximal small intestine. Eight rabbits with SFBL and seven nonoperated littermates were inoculated with RDEC-1 4 weeks after surgery. Semiquantitative estimation of fecal shedding of RDEC-1 and the presence and severity of diarrhea were monitored for 7 days. Rabbits were then killed, and colonization of jejunum and ileum by anaerobic bacteria and luminal colonization of jejunum, ileum, and cecum by RDEC-1 was quantitated. Mucosal adherence of RDEC-1 to jejunum, ileum, and cecum was determined by Giemsa staining of intestinal sections obtained from rabbits with and without SFBL. In addition, brush border membranes (BBM) were prepared from blind loop jejunum, nonoperated jejunum, and ileum. In vitro adherence of RDEC-1 to brush borders was quantitated under phase contrast microscopy. Maximal fecal shedding of RDEC-1 began 3-4 days after infection in all rabbits, but diarrhea was more severe in rabbits with SFBL.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Protective role of luteolin in 1,2-dimethylhydrazine induced experimental colon carcinogenesis.

The aim of the present study was to unravel the chemopreventive effect of luteolin on bacterial enzymes such as beta-glucuronidase and mucinase in a colon carcinogenesis model induced by 1, 2-dimethyl hydrazine (DMH). Twenty mg/kg body weight of DMH were administered subcutaneously once a week for the first 15 weeks and then discontinued. Luteolin (0.1, 0.2, or 0.3 mg/kg body weight/everyday (p.o.) was administered in a dose dependent manner at the initiation and also at the post-initiation stages of carcinogenesis to DMH treated rats. The animals were sacrificed at the end of 30 weeks. Colon cancer incidence and the activities of bacterial enzymes beta-glucuronidase (in the proximal colon, distal colon, intestines, liver and colon contents) and mucinase (colon and fecal contents) were significantly increased in DMH -treated rats compared to the control rats. On luteolin administration, colon cancer incidence, number of tumors per rat and the activities of beta-glucuronidase and mucinase, were significantly decreased both in the initiation and post-initiation stages of colon carcinogenesis dependent on the three different doses given. The increase in beta-glucuronidase activity may augment the hydrolysis of glucuronide conjugates, liberating toxins, while the increase in the mucinase activity may enhance the hydrolysis of the protective mucins in the colon. Thus our results demonstrate for the first time that luteolin, a dietary flavonoid, exerts chemopreventive and anticarcinogenic effects against DMH induced colon cancer.

1,2-Dimethylhydrazine↗
PubMed1988

Emergency laparotomy for spontaneous intestinal and colonic perforations in cancer patients receiving corticosteroids and chemotherapy.

Thirty patients with lymphoma (12), leukemia (two), myeloma (one), or metastatic solid tumors (15) were explored for 31 episodes of spontaneous intestinal perforation during an 11-year period at Memorial Sloan-Kettering Cancer Center. Twenty-three patients (76.6%) were receiving corticosteroids alone or in combination with chemotherapy and seven patients (23.4%) were receiving chemotherapy alone at the time of perforation. Fourteen perforations (45%) occurred in the small intestine and 17 perforations (55%) occurred in the colon. Malignancy was histologically demonstrated at the site of perforation in 16 patients (52%). Twenty major postoperative complications occurred in 15 patients (50%) and the operative mortality rate was 53%. Factors such as age, sex, duration or type of symptoms, site of perforation, malignancy at the site of perforation, peripheral leukocyte count, and serum albumin and total protein levels were not significantly related to patient survival. Early diagnosis and aggressive surgical intervention is essential to improve survival following intestinal perforation in this high-risk population.

Adrenal Cortex Hormones↗
PubMed1993

Thymic origin of embryonic intestinal gamma/delta T cells.

Current evidence suggests both thymic and extrathymic origins for T cells. Studies in mice favor an in situ origin for a prominent population of intestinal intraepithelial lymphocytes that express gamma/delta T cell receptor (TCR). This developmental issue is explored in an avian model in which the gamma/delta lymphocytes constitute a major T cell subpopulation that is accessible for study during the earliest stages of lymphocyte development. In the chick embryo, cells bearing the gamma/delta TCR appear first in the thymus where they reach peak levels on days 14-15 of embryogenesis, just 2 d before gamma/delta T cells appear in the intestine. Using two congenic chick strains, one of which expresses the ov antigen, we studied the origin and kinetics of intestinal colonization by gamma/delta T cells. The embryonic gamma/delta+ thymocytes homed to the intestine where they survived for months, whereas an embryonic gamma/delta- thymocyte population enriched in thymocyte precursors failed to give rise to intestinal gamma/delta+ T cells. Embryonic hemopoietic tissues, bone marrow, and spleen, were also ineffective sources for intestinal gamma/delta+ T cells. Intestinal colonization by gamma/delta+ thymocytes occurred in two discrete waves in embryos and newly hatched birds. The data indicate that intestinal gamma/delta T cells in the chicken are primarily thymic migrants that are relatively long-lived.

Age Factors↗
PubMed2003

Persistence of colonization of intestinal mucosa by a probiotic strain, Lactobacillus casei subsp. rhamnosus Lcr35, after oral consumption.

The colonization by the probiotic Lactobacillus casei subsp. rhamnosus Lcr35 of the gastrointestinal tracts of mice and humans was studied. The mice were orally given 10(9) CFU of Lcr35 either once or three times at 24-h intervals. A 16S ribosomal nucleic probe used in hybridization assays detected Lcr35 in the feces of mice for up to 3 days after the feeding, at a level of 10(8) to 10(9) CFU/g of feces. In the human assay, 12 healthy volunteers were enrolled in a randomized trial and ingested Lcr35 at a dosage of 10(8) or 10(10) or 10(12) CFU every day for 7 days. Then, after a 3-week posttreatment period, there was a second intake period similar to the first one. Analysis of fecal samples showed significant increases in the number of lactobacilli during the first intake period, whatever the dose given. The greatest increases were observed in subjects harboring the lowest indigenous population of Lcr35-like bacteria. During the 3-week posttreatment period, the number of CFU slightly decreased over time, and an increase, although not a statistically significant one, was observed during the second test period. These findings suggest that Lcr35 is able to survive within the gastrointestinal tract.

Administration, Oral↗
PubMed1997

Genetic and phenotypic characterization of intestinal spirochetes colonizing chickens and allocation of known pathogenic isolates to three distinct genetic groups.

Infection with intestinal spirochetes has recently been recognized as a cause of lost production in the poultry industry. Little is known about these organisms, so a collection of 56 isolates originating from chickens in commercial flocks in Australia, the United States, The Netherlands, and the United Kingdom was examined. Strength of beta-hemolysis on blood agar, indole production, API ZYM enzyme profiles, and cellular morphology were determined, and multilocus enzyme electrophoresis was used to analyze the extent of genetic diversity among the isolates. The results were compared with those previously obtained for well-characterized porcine intestinal spirochetes. The chicken isolates were genetically heterogeneous. They were divided into 40 electrophoretic types distributed among six diverse genetic groups (groups b to g), with a mean genetic diversity of 0.587. Strains in two groups (groups d and e) may represent new species of Serpulina, and the groups contained only strains isolated from chickens. Three genetic groups contained isolates previously shown to be pathogenic for chickens. These corresponded to the proposed species "Serpulina intermedius," to an unnamed group (group e), and to Serpulina pilosicoli. Two of the chicken isolates (one "S. intermedius" and one S. pilosicoli isolate) were strongly beta-hemolytic, two (both "S. intermedius") had an intermediate level of beta-hemolysis, and the rest were weakly beta-hemolytic. Fourteen isolates of "S. intermedius" produced indole, as did one isolate from group d. Isolates identified as S. pilosicoli resembled porcine isolates of this species, having four to six periplasmic flagella inserted subterminally in a single row at each end of the cell, and had tapered cell ends. All other spirochetes were morphologically similar, having seven or more periplasmic flagella and blunt cell ends. The identification of three genetic groups containing pathogenic isolates provides an opportunity for more detailed epidemiologic studies with these pathogens and for the development of improved diagnostic tests.

Animals↗
PubMed1980

Study of kinetics of epithelial cell populations in normal tissues of the rat's intestines and in carcinogenesis. I. A comparison of enterocyte population kinetics in different segments of the small intestine and colon.

The peculiarities of enterocyte proliferation in the duodenum, jejunum, ileum, caecum, ascending, transverse and descending colon in the rat were studied by different methods of analysis of cell population kinetics (percentage-labelled mitosis curves, cumulative labelling curves, distribution of labelling index curves, etc.). The majority of proliferating cells in the small intestine are homogenous, as far as mitotic cycle mean duration (11-12 hrs) is concerned. All proliferating cells in all the zones of the colonic crypts and the bottom of the small intestine crypts are divided into subpopulations, having different mean durations of the mitotic cycle. It is suggested that, in the crypt bottom in all intestines as well as the crypt's maximum proliferation zones in most of the colonic segments, a considerable fraction of cells has a very long mitotic cycle or enters resting phase R1. The average value of the mean durations of the mitotic cycle of all colonic enterocyte subpopulations is 18-22 hours. On the basis of the authors' findings and literature data, a model for the enterocyte life cycle is proposed, according to which the cell flux is branched during the mitotic cycle and the crypt develops from a stem enterocyte population located at its bottom.

Animals↗
PubMed1995

Immunohistochemical localization of guanylin in the rat small intestine and colon.

Guanylin is an endogenous mammalian ligand which binds to guanylate cyclase C (GC-C), the Escherichia coli heat-stable enterotoxin receptor. This interaction results in intestinal Cl- and fluid secretion, which is largely, if not exclusively, mediated through the cystic fibrosis transmembrane regulator (CFTR). Using in situ hybridization, we have previously localized guanylin mRNA to villus epithelial cells of the rat small intestine and to superficial epithelial cells of the rat colon. In the present study, we demonstrate immunoreactive guanylin in a subpopulation of goblet cells in the rat jejunum and ileum. In the colon, there was immunostaining of superficial epithelial cells and goblet cells. The immunohistochemical localization of guanylin parallels the observed distribution of guanylin mRNA. Localization of guanylin in goblet cells leads us to speculate that an in vivo function of guanylin regulated, CFTR-mediated Cl- secretion is to hydrate intestinal mucin.

Animals↗
PubMed2000

Differential role of cyclic GMP-dependent protein kinase II in ion transport in murine small intestine and colon.

BACKGROUND & AIMS: The aim of this study was to determine the role of guanosine 3',5'-cyclic monophosphate (cGMP)-dependent protein kinase (cGK) type II in intestinal fluid homeostasis under basal conditions and following exposure to cGMP-linked secretagogues, e.g., Escherichia coli heat-stable enterotoxin (STa) and guanylin. METHODS: Fluid and ion transport was determined in different segments of the intestine of wild-type and cGK II-deficient mice by ligated loop assays in vivo, and by short-circuit current and isotope flux measurements in vitro. RESULTS: Small intestinal fluid absorption in vivo was enhanced in cGK II-deficient mice under basal conditions and in the presence of STa. Furthermore, STa, guanylin, and 8-pCPT-cGMP stimulation of electrogenic anion secretion and inhibition of Na(+) absorption in vitro were markedly reduced in the small intestine from cGK II -/- mice but not in proximal colon. The type III phosphodiesterase inhibitor amrinone mimicked STa action in cGK II -/- mice, and also stimulated ion secretion in humans. CONCLUSIONS: This study shows that the cGMP/cGK II pathway regulates fluid homeostasis in the small intestine under basal conditions and mediates STa effects by both increasing anion secretion and inhibiting Na(+) absorption. It also demonstrates the presence of a cGK II-independent pathway for STa/cGMP-provoked secretion predominantly in the colon, which possibly involves a cGMP-inhibitable phosphodiesterase and/or activation of the cAMP-dependent protein kinase pathway.

Animals↗
PubMedDate not supplied

Colonization and persistence of Escherichia coli phenotypes in the intestines of children aged 0 to 18 months.

The aim of the present investigation was to study the intestinal colonization of Escherichia coli in newborn children, and to determine which strains become residential within the human intestine. The E. coli flora of 89 newborn children was studied by repeated sampling during their first 11 or 18 months of life. The E. coli isolates from the samples were subdivided into phenotypes by the aid of biochemical fingerprinting, a method which measures the kinetics of 24 selected biochemical tests as a tool for discriminating bacterial strains. It was found that E. coli strains colonizing children soon after birth persisted longer than strains colonizing them later. Especially those phenotypes which were defined as hospital strains persisted longer. Certain phenotypes were commonly found among the children, and these phenotypes were more persistent and more homogeneous than other phenotypes with respect to their pattern of biochemical activities. They might be specially adapted to colonize the human intestine. It was concluded that the generally long persistence of the first E. coli strains colonizing a newborn child indicates that the first case of bacterial colonization in children may be an event too important to be allowed to happen at random.

Aging↗
PubMed2000

Recombinant human interleukin-11 modulates ion transport and mucosal inflammation in the small intestine and colon.

Human recombinant interleukin 11 (rhIL-11) is a cytokine that suppresses the clinical signs of colitis in animal models of inflammatory bowel disease (IBD) and may be an effective therapeutic agent in the treatment of IBD. The objective of the current study was to investigate whether rhIL-11 was capable of reversing abnormalities in secretomotor function associated with gut inflammation. We investigated the effects of rhIL-11 on epithelial electrogenic ion transport in the jejunum and colon. Application of rhIL-11 (10 to 10,000 ng/ml) at either the luminal or serosal side of mucosal sheets isolated from control rats induced a concentration-dependent reduction of transmural potential difference (PD) in the jejunum and decreased the short-circuit current (Isc), representative of active electrogenic transport, in the colon. To investigate the effect of rhIL-11 on an inflamed gut, we isolated jejunal and colonic tissue from HLA-B27 transgenic rats with active inflammation of the bowel that represents an animal model of IBD. In jejunum and colon isolated from HLA-B27 transgenic rats, basal electrogenic ion transport was significantly attenuated and, under these conditions, rhIL-11 caused no changes in either transmural PD or Isc. However, in HLA-B27 rats, pretreatment with subcutaneous doses of rhIL-11 suppressed the symptoms of diarrhea, normalized myeloperoxidase activity in the jejunum and colon and healed mucosal injury. In the jejunum from HLA-B27 rats, healing of the intestinal inflammatory response enhanced basal transmural PD and the rhIL-11-duced changes in mucosal ion transport resembled those seen in uninflamed controls. Conversely, in the colon, healing of the mucosa did not normalize basal active ion transport nor did it reverse the inhibition of rhIL-11-induced changes in colonic Isc. Our results suggest that endogenous IL-11 may act as a modulator of epithelial transport under physiologic conditions and may act as a potent anti-inflammatory cytokine during active intestinal inflammation.

Animals↗
PubMed1993

Tissue and cell-specific patterns of expression of rat liver and intestinal fatty acid binding protein during development and in experimental colonic and small intestinal adenocarcinomas.

BACKGROUND: Mammalian small intestinal and colonic epithelium express members of a multigene family of hydrophobic ligand binding proteins of which liver and intestinal fatty acid binding protein represent among the most abundant intestinal gene products. These proteins are expressed in a cell- and region-specific manner and emerge in a temporally distinctive pattern. EXPERIMENTAL DESIGN: We have studied expression of these genes in the small intestine and colon of rats treated with 1,2-dimethylhydrazine since these animals develop a predictable pattern of both small and large bowel cancers. Studies were also undertaken in fetal and neonatal small intestine and colon. RESULTS: There was a 10- and 50-fold decrease, respectively, in mRNA abundance for intestinal and liver fatty acid binding protein in RNA from colon cancers compared with either uninvolved or control RNA. Immunocytochemical analysis revealed decreased staining for both proteins within their normal distribution together with ectopic clusters of cells reactive for liver fatty acid binding protein within colonic tumors. A more striking mosaic of immunocytochemical staining for both liver and intestinal fatty acid binding protein was found in small intestinal adenocarcinomas. Similar mosaic patterns of immunocytochemical staining were transiently detectable in rat fetal small intestine and neonatal colon. CONCLUSIONS: The region- and cell-specific expression of these genes, which may be linked temporally to events in intestinal differentiation, are subject to disruption in a cell-specific manner in the transformed, or dedifferentiated, phenotype.

1,2-Dimethylhydrazine↗
PubMed2003

Fenugreek affects the activity of beta-glucuronidase and mucinase in the colon.

The effect of fenugreek seeds on the activities of beta-glucuronidase and mucinase during 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in rats was studied. Rats were given a weekly subcutaneous injection of DMH at a dose of 20 mg/kg body weight, for 15 weeks. Fenugreek seed powder was weighed depending upon the weight of individual rats and incorporated in the powdered pellet diet at a dose of 2 g/kg body weight. After an experimental period of 30 weeks the activity of beta-glucuronidase significantly increased in the colon, intestine, liver and colon contents in DMH administered rats when compared to an untreated control group. Increase in beta-glucuronidase may increase the hydrolysis of carcinogen-glucuronide conjugate, liberating carcinogen and/or co-carcinogen within the colonic lumen. Inclusion of fenugreek seed powder in the diet significantly decreased the activity of beta-glucuronidase in all the tissues studied. This may prevent the free carcinogens from acting on colonocytes. Mucinase helps in hydrolysing the protective mucin. Mucinase activity was increased in the colon content and fecal content of animals given DMH when compared to control, while the activity was significantly reduced in animals given DMH + fenugreek when compared to animals given DMH only. Our study shows that supplementation of fenugreek seeds in the diet inhibits colon carcinogenesis, by modulating the activities of beta-glucuronidase and mucinase. The beneficial effect may be attributed to the presence of fibre, flavonoids and/or saponins.

1,2-Dimethylhydrazine↗
PubMed2026

In vivo CRISPRi screens reveal Escherichia coli functional adaptations in the mouse gut.

Escherichia coli exhibits remarkable genetic diversity that enables it to adapt to the intestinal environment. Here we establish an in vivo CRISPR interference platform that leverages bacterial gene fitness as a high-resolution functional reporter of E. coli adaptations within mice harbouring a defined minimal microbial community (OligoMM12). The screen revealed that diet profoundly shapes the metabolic landscape of E. coli and the essential gene profile identified cross-feeding interactions. Comparison between a laboratory strain (MG1655), a uropathogenic strain (CFT073) and an adherent-invasive E. coli (AIEC LF82) identified distinct genetic requirements for intestinal colonization, highlighting divergent motility, stress response and respiration strategies. In a host inflammatory environment, we found that AIEC LF82 preferably colonized the small intestine with a mobile genetic element, Gally prophage, playing an important role in modulating fitness. These findings provide a high-resolution genetic atlas of E. coli's functional adaptation and demonstrate the utility of functional genomics to probe the gut environment itself.

Journal Article↗