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PubMedDate not supplied

Altered colonizing ability for the ceca of broiler chicks by lipopolysaccharide-deficient mutants of Salmonella typhimurium.

Salmonella typhimurium strain 3333/O was used to assess the role of bacterial lipopolysaccharide (LPS) in intestinal colonization of broiler chicks by salmonellae. LPS-defective TnPhoA mutants of this strain were isolated. The sensitivities of the mutants to smooth and rough phages and LPS banding patterns in sodium dodecyl sulfate-polyacrylamide gel electrophoresis indicated a defect in the polysaccharide side chain of the LPS molecule. Colonization was determined by orally administering 10(8) cells each of the wild-type and/or the mutant strains per chick and counting the colony-forming units (CFU) from the ceca 1 to 3 weeks after gavage. CFU of chicks given the LPS-deficient strains either were not detected or were significantly lower than the CFU from chicks given the wild-type strain. The incidence of the wild-type strain in spleens was higher than incidence of the mutant strains. In vitro binding studies with LPS-deficient mutants derived in this study and from S. typhimurium LT2 suggest that LPS side-chain components may shield the bacterial cell from entrapment in the chicken mucus. The LPS layer appears to enhance persistence of Salmonella in the avian intestinal tract.

Animals↗
PubMed1998

Targeted disruption of the mouse villin gene does not impair the morphogenesis of microvilli.

The small intestine is functionally dependent on the presence of the brush border, a tightly packed array of microvilli that forms the amplified apical surface of absorptive cells. In the core of each microvillus, actin filaments are bundled by two proteins, villin and fimbrin. Previous in vitro studies using antisense approaches indicated that villin plays an important role in the morphogenesis of microvilli. To examine the in vivo consequences of villin deficiency, we disrupted the mouse villin gene by targeted recombination in mouse embryonic stem cells. A beta-galactosidase cDNA was also introduced into the villin locus by the targeting event. Homozygous villin-deficient mice are viable, fertile, and display no gross abnormalities. Intact microvilli are present in the small intestine, colon, kidney proximal tubules, and liver bile canaliculi. Although subtle ultrastructural abnormalities can be detected in the actin cores of small intestinal microvilli, localization of sucrase isomaltase, brush border myosin I, and zonula occludens I to the microvillar surface of the small intestine is normal. Thus, in vivo, villin plays a minor or redundant role in the generation of microvilli in multiple absorptive tissues.

Animals↗
PubMed1999

Prevalence and infection risks of zoonotic enteropathogenic bacteria in Swiss cow-calf farms.

A longitudinal study was performed in 67 larger Swiss cow-calf farms from September 1996 through November 1997. The objectives of the study were to estimate prevalence and risk factors for colonization with potentially zoonotic enteropathogenic bacteria in younger calves and in calves at weaning age. The study included data from 395 calves with three to four fecal samples each. Fecal samples were analyzed for Campylobacter spp., verotoxin producing E. coli (VTEC), Yersinia spp. and Salmonella sp. Possible environmental and individual factors associated with colonization of these agents were examined. The calves were housed indoor during the first 3 months of life (winter 1996/1997). The prevalences within this time period were: C. coli 3.4%, C. fetus 15.5%, C. hyointestinalis 9.6%, C. jejuni 38.5%, VTEC 44.3% and Yersinia spp. 2%. At the end of the grazing season the prevalences at weaning (8-10 months of age) were: C. coli 1.7%, C. fetus 4.0%, C. hyointestinalis 25.9%, C. jejuni 13.3%, VTEC 38.2% and Yersinia spp. 0%. No salmonellae were present at any time of the study. The prevalences of C. jejuni and VTEC increased significantly within the first 3 months of life, whereas C. hyointestinalis decreased. None of the environmental factors such as housing or feeding had any consistent influences on colonization by the bacteria studied. VTEC, Campylobacter spp. and Yersinia spp. should probably be considered as normal inhabitants of the bovine intestinal tract. However, as they represent a source of gastrointestinal infections in humans, management factors limiting intestinal colonization of these bacteria should be considered in cow-calf operations.

Agglutination Tests↗
PubMed1990

Alterations in splanchnic blood flow following chronic ethanol exposure.

The purpose of these experiments was to determine whether or not tolerance develops to the effect of 3.0 g/kg ethanol on total and regional splanchnic blood flow in male Wistar rats. The animals were given the Lieber-DeCarli liquid diet containing ethanol for 10 days; ethanol-fed animals were withdrawn 24 hr prior to experiments. Regional blood flow and cardiac output (CO) were measured by the reference microsphere technique after an intraperitoneal injection of 3.0 g/kg of ethanol. Acute ethanol administration produced early nonsustained increases in portal vein blood flow in animals fed ethanol for 10 days and withdrawn for 24 hr and in control animals. However, after chronic exposure to ethanol, the pattern of increase in blood flow in response to ethanol in the splanchnic organs was different between the ethanol-fed and control groups. Increases in portal vein flow in control groups were due to concomitant increases in small intestinal, colonic, and cecal blood flow while the increase in the ethanol-fed group was due to a rise in small intestinal and stomach blood flow. The increase in stomach blood flow that occurred in the animals treated chronically with ethanol may be viewed as a conditioned response to ethanol, since this was not found in the control group. These results, demonstrate that the pattern of increase in blood flow in the splanchnic organs produced by an acute dose of ethanol depends on the animal's previous exposure to ethanol.

Alcohol Withdrawal Delirium↗
PubMed1989

Purification and analysis of colonization factor antigen I, coli surface antigen 1, and coli surface antigen 3 fimbriae from enterotoxigenic Escherichia coli.

Enterotoxigenic Escherichia coli fimbriae are immunogenic and play a key role in intestinal colonization. Native colonization factor antigen I, coli surface antigen 1, and coli surface antigen 3 fimbriae were purified by a common method involving shearing, differential centrifugation, gel filtration, and density gradient ultracentrifugation. The compositions and N-terminal sequences were determined. Coli surface antigen 3 possesses two N-terminal isoforms, one of which matches the published DNA sequence, except for the previously proposed signal sequence cleavage point.

Amino Acid Sequence↗
PubMed2001

Antibodies to CD40 induce a lethal cytokine cascade after syngeneic bone marrow transplantation.

CD40 stimulation, by either antibody or ligand, has been shown to inhibit the growth of a variety of neoplastic cells, both in vivo and in vitro. In this study, we assessed the effects of CD40 stimulation using a murine agonistic CD40 monoclonal antibody (MoAb) (FGK115) or a soluble recombinant murine CD40 ligand (srmCD40L) in both lethally irradiated and nonirradiated BALB/c mice. Toxicity after CD40 stimulation was not observed in nonirradiated animals receiving up to 100 microg of the agonist anti-CD40 MoAb. However, as little as 10 microg of the agonistic anti-CD40 MoAb induced acute toxicity resulting in 100% morbidity of lethally irradiated animals by 4 days after irradiation. Histological evaluation of animals receiving anti-CD40 MoAb revealed severe intestinal lesions with disruption of the villi, goblet cell depletion, and crypt hyperplasia of the small intestine, colon, and cecum. Delaying the administration of anti-CD40 MoAb or reducing the amount of irradiation given resulted in increased survival and less severe lesions. Analysis of serum cytokine levels in lethally irradiated mice receiving agonistic anti-CD40 showed a marked increase of interferon (IFN)-gamma. Lethally irradiated IFN-gamma knockout mice given the agonistic anti-CD40 MoAb demonstrated significant increases in survival and minimal gut lesions compared with wild-type mice receiving the same regimen, suggesting that IFN-gamma plays a major role in this toxic reaction. These results indicate that CD40 stimulation using agonistic antibodies following lethal irradiation leads to a fatal, cytokine-induced disease affecting the intestine.

Animals↗
PubMed1998

Identification of Salmonella typhimurium genes required for colonization of the chicken alimentary tract and for virulence in newly hatched chicks.

From a collection of 2,800 Tn5-TC1 transposon mutants of Salmonella typhimurium F98, 18 that showed reduced intestinal colonization of 3-week-old chicks were identified. The sites of transposon insertion were determined for most of the mutants and included insertions in the lipopolysaccharide biosynthesis genes rfaK, rfaY, rfbK, and rfbB and the genes dksA, clpB, hupA, and sipC. In addition, identification was made of an insertion into a novel gene that encodes a protein showing similarity to the IIC component of the mannose class of phosphoenolpyruvate-carbohydrate phosphotransferase systems, which we putatively called ptsC. Transduction of most of the transposon mutations to a fresh S. typhimurium F98 genetic background and construction of defined mutations in the rfbK, dksA, hupA, sipC, and ptsC genes of S. typhimurium F98 supported the role in colonization of all but the pts locus. The virulence of the rfbK, dksA, hupA, sipC, and ptsC defined mutants and clpB and rfaY transductants in 1-day-old chicks was tested. All but the ptsC and rfaY mutants were attenuated for virulence. A number of other phenotypes associated with some of the mutations are described.

Animals↗
PubMed1999

Edema disease as a model for systemic disease induced by Shiga toxin-producing E. coli.

Edema disease (ED) is a naturally occurring disease of weaned pigs caused by host adapted strains of E. coli that produce Shiga toxin (STEC). We determined the temporal and quantitative relationships between intestinal colonization by STEC, levels of Shiga toxin (Stx2e) in the gut, in the blood, and clinical manifestations of ED. Bacterial colonization (10(8) CFU/cm ileum) was highest 4 days post inoculation (pi) in animals that did not develop clinical disease and 6 days pi in animals with clinical signs of ED. The mean time for the development of clinical signs of ED was 6 days pi (range 4-10). Average peak titers of Stx2e in the ileum were 1:16,384 in asymptomatic animals and 1:32,768 in clinical animals. Titers of Stx2e in the feces reflected the toxin titers in the ileum but were lower. Intestinal titers of Stx2e and the density of bacterial colonization were predictive of clinical ED for a group of animals but not for individuals. Approximately 50% of the pigs that had Stx2e titers of > or = 1:4096 and a bacterial density of > or = 10(6) CFU/cm in their ileum, had clinical ED. Pigs that had intestinal Stx2e titers < 1:4096 were asymptomatic. Stx2e was detected in the red cell fraction of blood from some of the pigs with clinical ED and in some that were asymptomatic. Stx2e was not detected in the serum of any animals. ED may be a useful model for predicting the temporal and quantitative relationships between bacterial colonization, Stx levels in the gut and blood and systemic disease for STEC in other species.

Animals↗
PubMed2004

Cloning and functional characterization of the human GLUT7 isoform SLC2A7 from the small intestine.

Facilitated glucose transporters (GLUTs) mediate transport of sugars across cell membranes by using the chemical gradient of sugars as the driving force. Improved cloning techniques and database analyses have expanded this family of proteins to a total of 14 putative members. In this work a novel hexose transporter isoform, GLUT7, has been cloned from a human intestinal cDNA library by using a PCR-based strategy (GenBank accession no. AY571960). The encoded protein is comprised of 524 amino acid residues and shares 68% similarity and 53% identity with GLUT5, its most closely related isoform. When GLUT7 was expressed in Xenopus oocytes, it showed high-affinity transport for glucose (K(m) = 0.3 mM) and fructose (IC(50) = 0.060 mM). Galactose, 2-deoxy-d-glucose, and xylose were not transported. Uptake of 100 microM d-glucose was not inhibited by 200 microM phloretin or 100 microM cytochalasin B. Northern blotting indicated that the mRNA for GLUT7 is present in the human small intestine, colon, testis, and prostate. Western blotting and immunohistochemistry of rat tissues with an antibody raised against the predicted COOH-terminal sequence confirmed expression of the protein in the small intestine and indicated that the transporter is predominantly expressed in the enterocytes' brush-border membrane. The unusual substrate specificity and close sequence identity with GLUT5 suggest that GLUT7 represents an intermediate between class II GLUTs and the class I member GLUT2. Comparison between these proteins may provide key information as to the structural determinants for the recognition of fructose as a substrate.

Amino Acid Sequence↗
PubMed1983

Crohn's disease in the elderly.

Surgical procedures for Crohn's disease of the small intestine, colon, or rectum were performed in 25 patients who were 65 years of age or older. In elderly patients with primarily small-bowel disease, good results were obtained uniformly by ileal resection and primary intestinal anastomosis. In 15 patients, Crohn's disease involved primarily the large intestine. Subtotal abdominal colectomy with end ileostomy restored health and permitted weight gain in six patients, although three required subsequent proctosigmoidectomy for recurrent rectal symptoms (average interval--18 months). Four patients underwent one-stage proctocolectomy, with one postoperative death and delayed healing of the perineal wound in the three survivors. Major complications frequently followed surgical procedures for suspected sigmoid diverticulitis in elderly patients with unrecognized Crohn's disease of the colon.

Adult↗
PubMed1986

In vivo induction of H-2K/D antigens by recombinant interferon-gamma.

B10.BR mice received i.v. increasing doses of recombinant interferon-gamma (rIFN-gamma) on three consecutive days. Using an immunoperoxidase technique the distribution of H-2K/D antigens was studied in frozen tissue sections of thirteen organs (kidney, liver, pancreas, esophagus, stomach, small intestine, colon, lungs, heart, brain, thymus, lymph node and spleen). Class I antigens were shown to be induced or enhanced in almost every organ after exposure to IFN-gamma. This effect was particularly conspicuous for renal tubular cells, hepatocytes, bronchiolar epithelial cells, gastric mucous cells, thymic cortical lymphocytes and capillary endothelial cells in heart and kidney. Neurons, glial cells, gastric chief and parietal cells, and pancreas cells were not inducible. The findings show that i.v. application of IFN-gamma leads to strong induction or enhancement of major histocompatibility complex class I antigens in a wide variety of tissues.

Antibodies, Monoclonal↗
PubMed1995

Monocyte-chemoattractant protein 1 gene expression in intestinal epithelial cells and inflammatory bowel disease mucosa.

BACKGROUND: Monocyte-chemoattractant protein 1 (MCP-1) activates macrophages and increases the migration of monocytes into tissue during inflammation. It was hypothesized that MCP-1 expression is involved in intestinal inflammation. METHODS: MCP-1 protein was detected by immunohistochemistry and immunoprecipitation. Biological activity of MCP-1 was assessed using a chemotactic assay. MCP-1 messenger RNA (mRNA) levels were measured by quantitative reverse-transcription polymerase chain reaction. RESULTS: In normal mucosa, MCP-1 was predominantly present in surface epithelium. In contrast, inflamed mucosa from patients with ulcerative colitis or Crohn's disease contained multiple cells immunoreactive for MCP-1, including spindle cells, mononuclear cells, and endothelial cells. Furthermore, MCP-1 mRNA expression was markedly increased in inflamed intestinal biopsy specimens from patients with inflammatory bowel disease. MCP-1 was detected in isolated intestinal epithelial cells and in conditioned media from Caco-2 cells. Caco-2 cell-conditioned media stimulated monocyte chemotaxis activity that was inhibited by anti-MCP-1 antibodies. Constituitive MCP-1 mRNA levels in Caco-2 cells were up-regulated by interleukin 1 beta and down-regulated by dexamethasone. CONCLUSIONS: In addition to lamina propria macrophages, endothelial cells, and spindle cells, intestinal epithelial cells are able to produce MCP-1. MCP-1 is expressed constitutively in the intestinal colonic mucosa and is up-regulated during inflammation.

Base Sequence↗
PubMedDate not supplied

Role of extrinsic innervation in release of motilin and patterns of upper gut canine motility.

The need for extrinsic neural input to the upper gut in regulation/control of cyclic interdigestive motility and release of motilin remains a topic of controversy. Our aim was to determine whether extrinsic denervation of the upper gut disrupts cyclic release of motilin in relation to the migrating motor complex. Ten dogs underwent transection of all extrinsic innervation and enteric neural input to the stomach, small intestine, colon, pancreas, and liver while enteric neural continuity within this multivisceral complex was maintained. A cyclic pattern of motility occurred during fasting in all dogs in the small bowel (period = 100 +/- 3 min, mean +/- standard error of the mean) and in 8 of 10 dogs in the stomach (period = 98 +/- 4 min). Gastric cycles were temporally coordinated with small bowel cycles. Plasma motilin concentrations cycled temporally with the motility pattern with the greatest concentrations occurring during gastroduodenal phase III-like activity. Exogenous motilin induced a burst of gastric contractions and a premature migrating motor complex in all dogs. Oral meals disrupted cyclic motility and cyclic changes in plasma motilin. Extrinsic innervation to the upper gut is not necessary for cyclic motor activity, for coordinated cyclic release of motilin, or to initiate a premature migrating motor complex-like response to motilin. Central nervous system input (afferent, efferent) is not necessary for cyclic interdigestive activity or cyclic release of motilin.

Afferent Pathways↗
PubMed2006

Dietary fructooligosaccharides affect intestinal barrier function in healthy men.

In contrast to most expectations, we showed previously that dietary fructooligosaccharides (FOS) stimulate intestinal colonization and translocation of invasive Salmonella enteritidis in rats. Even before infection, FOS increased the cytotoxicity of fecal water, mucin excretion, and intestinal permeability. In the present study, we tested whether FOS has these effects in humans. A double-blind, placebo-controlled, crossover study of 2 x 2 wk, with a washout period of 2 wk, was performed with 34 healthy men. Each day, subjects consumed lemonade containing either 20 g FOS or placebo and the intestinal permeability marker chromium EDTA (CrEDTA). On the last 2 d of each supplement period, subjects scored their gastrointestinal complaints on a visual analog scale and collected feces and urine for 24 h. Fecal lactic acid was measured using a colorimetric enzymatic kit. The cytotoxicity of fecal water was determined with an in vitro bioassay, fecal mucins were quantified fluorimetrically, and intestinal permeability was determined by measuring urinary CrEDTA excretion. In agreement with our animal studies, FOS fermentation increased fecal wet weight, bifidobacteria, lactobacilli, and lactic acid. Consumption of FOS increased flatulence and intestinal bloating. In addition, FOS consumption doubled fecal mucin excretion, indicating mucosal irritation. However, FOS did not affect the cytotoxicity of fecal water and intestinal permeability. The FOS-induced increase in mucin excretion in our human study suggests mucosal irritation in humans, but the overall effects are more moderate than those in rats.

Adult↗
PubMed1997

First report of invasive amebiasis in an organ transplant recipient.

T-cell mediated immunity is an important defense mechanism against amebiasis. However, organ transplant recipients with severe T-cell immunosuppression are not at increased risk of having Entamoeba histolytica invasive disease. The reasons are unclear and probably multifactorial, but it is likely that the absence of intestinal colonization with pathogenic strains in countries where transplants occur and the judicious intake of possible contaminated food and water are important contributing factors. We describe the first report of a liver transplant recipient with severe E. histolytica colitis who was successfully treated with metronidazole without modifying his immunosuppression therapy.

Adult↗
PubMed1997

Aggregative adherence fimbria II, a second fimbrial antigen mediating aggregative adherence in enteroaggregative Escherichia coli.

Enteroaggregative Escherichia coli (EAEC) has been implicated as an agent of pediatric diarrhea in the developing world. We have shown previously that EAEC adheres to HEp-2 cells by virtue of a plasmid-encoded fimbrial adhesin designated aggregative adherence fimbria I (AAF/I), the genes for which have been cloned and sequenced. However, not all EAEC strains express AAF/I. Using TnphoA mutagenesis, we have characterized a novel fimbria (designated AAF/II) which mediates HEp-2 adherence of the human-pathogenic strain 042. AAF/II is 5 nm in diameter and does not bind AAF/I antiserum, as determined by immunogold transmission electron microscopy. TnphoA identified a gene (designated aafA) which bears significant homology to aggA, the fimbrial subunit of AAF/I (25% identity and 47% similarity at the amino acid level). When hyperexpressed and purified by polyhistidine tagging, the AafA protein assembled into 5-nm-diameter filaments which bound anti-AAF/II antiserum. The cloned aafA gene complemented a mutation in the aggA gene to confer fimbrial expression from the AAF/I gene cluster, manifesting phenotypes characteristic of AAF/II but not AAF/I. The aafA mutant did not adhere to human intestinal tissue in culture, suggesting a role for AAF/II in intestinal colonization. By using DNA probes for AAF/I and AAF/II derived from fimbrial biosynthesis genes, we show that AAF/I and AAF/II are each found in only a minority of EAEC strains, suggesting that still more EAEC adhesins exist. Our data suggest that AAF adhesins represent a new family of fimbrial adhesins which mediate aggregative adherence in EAEC.

Adhesins, Escherichia coli↗
PubMed1993

[Intestinal receptors for adhesive fimbriae of Escherichia coli in swine--a literature review].

This review describes the mechanism of intestinal colonization by enterotoxigenic and enterotoxaemic Escherichia (E.) coli in swine. Colonization depends on specific binding between adhesive fimbriae and receptors on the enterocytes. Special focus is given on the occurrence of specific intestinal receptors for the fimbrial antigens F4 (K88), F5 (K99), F6 (987P) and F41. The demonstration of these receptors allows the identification of susceptible and resistant pigs. Furthermore unclassified adhesive fimbriae of E. coli isolated from pigs with postweaning diarrhea and edema disease are described. Finally the present knowledge is discussed in context with protection of animals against infections.

Animals↗
PubMed1989

[The effect of previous antibiotherapy on the colonization of an Escherichia coli strain sensitive to antibiotics in the digestive tract of hospitalized children].

The administration of the Escherichia coli (az) strain has already been used successfully to protect premature infants against intestinal colonization by nosocomial strains of antibiotic resistant enteric organisms. The purpose of the present study was to assess the protective value of this strain in older full term babies after cessation of an antibiotics treatment. Two groups of children treated with antibiotics of respectively 8-90 days and 3-12 months of age were studied and compared to two control groups of untreated children. In both groups of children, the implantation of E. coli az was higher in treated than in untreated subjects. The group of younger children was significantly less colonized by antibiotic resistant hospital acquired enteric organisms, whereas in 3-12 months old children non protective effect of E. coli az was recorded. Therefore, the antagonistic effect of the strain studied appeared as age dependent.

Anti-Bacterial Agents↗