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At least 649 records · Page 36Linked to original sources
PubMed1979

The gastrointestinal absorption of paracetamol in the rat.

The absorption of [3H]paracetamol by rat small intestine, colon and stomach was studied in vivo and in vitro. Small intestinal in vivo studies, using a wide range of drug concentrations, showed that absorption was efficient and uniform throughout the small bowel, no site showing preferential absorption. Double reciprocal and direct plots indicated first order kinetics. The pattern was not observed when uptake was occurring from high concentrations of paracetamol in suspension. Gastric and colonic in vivo studies showed that there was appreciable absorption of [3H]paracetamol from these sites. In vitro studies using everted intestinal sacs showed no effect on paracetamol transfer when the incubation temperature was lowered to 10 degrees C or when iodoacetate (5 X 10(-2)M) and 2.4 dinitrophenol (5 X 10(-4)M) was added to the incubation medium. There was, however, a significant reduction in transfer of paracetamol against a concentration gradient of 10:1 applied across the mucosa. These data suggest that the uptake of paracetamol is by a passive transport process and confirm the efficiency of paracetamol absorption observed indirectly by others.

Acetaminophen↗
PubMed1999

Intestinal mucins in colonization and host defense against pathogens.

Intestinal mucins are key components of the first line of host defense against intestinal pathogens. These large glycoconjugates secreted by specialized exocrine goblet cells form viscous gels that trap microorganisms and irritants and limit their diffusion to the intestinal epithelium. Moreover, they allow for colonization by indigenous bacterial flora that prevents attachment of pathogenic microbes. The interaction between microbes and mucins involves mucin carbohydrate side chains and microbial adhesin molecules. Certain microorganisms and disease states may alter mucin biochemistry or expression. Although these alterations most likely contribute to disease processes, the full impact of these phenomena are still unclear. The development of mucin-secreting cell lines has facilitated the study of mucin biology and aided our understanding of mucin-microbial interactions.

Animals↗
PubMed1995

Immunogenicity and protective efficacy of a prototype Campylobacter killed whole-cell vaccine in mice.

The immunogenicity and efficacy of an experimental inactivated Campylobacter jejuni whole-cell (CWC) vaccine were evaluated in mice. Mice were orally immunized in a three-dose primary series (48-h intervals) at doses of 10(5), 10(7), or 10(9) CWC vaccine particles alone or in combination with 25 micrograms of a mucosal adjuvant, the heat-labile enterotoxin of Escherichia coli (LT). The comparative immunogenicities of both formulations were assessed on the basis of the generation of antigen-specific antibodies in serum and intestinal secretions, and efficacy was determined by measuring the degrees of protection afforded against intestinal colonization and systemic dissemination of challenge organisms. Campylobacter-specific intestinal immunoglobulin (Ig) A responses were dependent on the use of LT, whereas IgA and IgG responses in serum were not. Colonization resistance was induced over a broad range of vaccine doses when LT was included. However, only the highest dose of CWC alone gave comparable levels of protection. Both formulations provided equivalent protection against systemic spread of challenge organisms. These results indicate that both whole-cell vaccine formulations deserve further evaluation as candidate vaccines and also highlight the potential value of mucosal adjuvants, like LT, in enteric vaccine development.

Animals↗
PubMed1995

Lamina propria T cell subsets in the small and large intestine of euthymic and athymic mice.

We investigated lamina propria T cells from the small intestine (jejunum/ileum) and the large intestine (colon) of euthymic (BALB/c, C.B-17, C57BL/6) and athymic (C57BL/6 nu/nu; BNX bg/bg nu/nu xid/xid) mice. CD3+ T cells represented about 40% of the lamina propria lymphocytes (LPL) from the small or the large intestine of euthymic mice, and 20-30% of the LPL populations from the small or large intestine of athymic mice. In the lamina propria T cell population of the small intestine, 85% were of the alpha beta lineage in euthymic mice, but only 40% were of the alpha beta lineage in athymic mice. T cells of the gamma delta lineage were thus more frequent than T cells of the alpha beta lineage in the intestinal lamina propria T cells of extrathymic origin. CD4+ T cells represented 40% of the lamina propria T cells in the small as well as in the large intestine of euthymic mice, and 20-30% of the T cells in the lamina propria of the nude mouse gut. In euthymic mice, 40% of the T cells in the small intestine lamina propria, and 30% of the T cells in the colonic lamina propria were CD8+. In intestinal lamina propria T cell populations of athymic mice, the CD8+ T cell population was expanded. Most (60-70%) CD8+ T cells in the lamina propria of the small and the large intestine of euthymic and athymic mice expressed the homodimeric CD8 alpha + beta- form of the CD8 coreceptor. A fraction of 15-20% of all CD3+ T cells in the lamina propria of the small and the large intestine of euthymic and athymic mice were 'double negative' CD4- CD8-. A large fraction of the TCR alpha beta + T cells in the colonic lamina propria (but not in the small intestine lamina propria) of euthymic mice expressed the CD2 and the CD28 costimulator molecules, the adhesion molecule LECAM-1 (CD62 L), and could be activated in vitro by CD3 ligation. These data reveal a considerable heterogeneity in the surface phenotype and the functional phenotype of murine lamina propria T cells.

Animals↗
PubMed1994

Identification of I-plastin, a human fimbrin isoform expressed in intestine and kidney.

The complete cDNA sequence of human intestine-specific plastin (I-plastin) was determined from a clone derived by PCR. It consists of a 97-bp 5' untranslated region, a 1,887-bp coding region, and a 1,655-bp 3' untranslated region. The coding region predicts a 629-residue polypeptide whose sequence displays 86, 75, and 73% identities with chicken intestine fimbrin, human T-plastin, and human L-plastin, respectively. Recombinant I-plastin cross-linked actin filaments into bundles in the absence but not in the presence of calcium. The I-plastin gene was mapped by PCR to human chromosome 3; the L- and T-plastin genes were previously mapped to chromosomes 13 and X, respectively. I-plastin mRNA was detected in the small intestine, colon, and kidneys; relatively lower levels of expression were detected in the lungs and stomach. In contrast, L-plastin expression was restricted to the spleen and other lymph node-containing organs, while T-plastin was expressed in a variety of organs, including muscle, brain, uterus, and esophagus. In contrast to the situation for the intestine, high levels of L- and T-plastin mRNAs were detected in Caco-2, a human colon-derived cell line. Immunofluorescence microscopy detected I-plastin in the brush border of the small intestine and colon. These results identify I-plastin as the human homolog of chicken intestine fimbrin and as a third plastin isoform in humans.

Amino Acid Sequence↗
PubMed2000

Investigation of the role of type IV Aeromonas pilus (Tap) in the pathogenesis of Aeromonas gastrointestinal infection.

Although there is substantial evidence that type IV pili purified from diarrhea-associated Aeromonas species (designated Bfp for bundle-forming pilus) are intestinal colonization factors (S. M. Kirov, L. A. O'Donovan, and K. Sanderson, Infect. Immun. 67:5447-5454, 1999), nothing is known regarding the function of a second family of Aeromonas type IV pili (designated Tap for type IV Aeromonas pilus), identified following the cloning of a pilus biogenesis gene cluster tapABCD. Related pilus gene clusters are widely conserved among gram-negative bacteria, but their significance for virulence has been controversial. To investigate the role of Tap pili in Aeromonas pathogenesis, mutants of Aeromonas strains (a fish isolate of A. hydrophila and a human dysenteric isolate of A. veronii bv. sobria) were prepared by insertional inactivation of the tapA gene which encodes the type IV pilus subunit protein, TapA. Exotoxic activities were unaffected by the mutation in tapA. Inactivation of tapA had no effect on the bacterial adherence of these two isolates to HEp-2 cells. For the A. veronii bv. sobria isolate, adhesion to Henle 407 intestinal cells and to human intestinal tissue was also unaffected. There was no significant effect on the duration of colonization or incidence of diarrhea when the A. veronii bv. sobria strain was tested in the removable intestinal tie adult rabbit diarrhea model or on its ability to colonize infant mice. Evidence was obtained that demonstrated that TapA was expressed by both Aeromonas species and was present on the cell surface, although if assembled into pili this pilus type appears to be an uncommon one under standard bacterial growth conditions. Further studies into factors which may influence Tap expression are required, but the present study suggests that Tap pili may not be as significant as Bfp pili for Aeromonas intestinal colonization.

Aeromonas↗
PubMed1978

Colonization resistance of the digestive tract and gastrointestinal transit time in SPF mice.

The gastro-intestinal colonization resistance to Escherichia coli was assessed in individual CBA/Rij, C3H/StZ and Swiss/Cpb:SE mice. Gastro-intestinal transit time was determined by feeding small steel balls and x-ray examination of sequentially collected faeces. No correlation was found between transit times measured on 3 subsequent days, nor between them and colonization resistance.

Animals↗
PubMed2003

The early increase in intestinal permeability and systemic endotoxin exposure in patients with severe acute pancreatitis is not associated with systemic bacterial translocation: molecular investigation of microbial DNA in the blood.

INTRODUCTION: Sepsis is the main cause of late mortality in patients with severe acute pancreatitis and is largely attributed to secondary infection of pancreatic necrosis with gram-negative enteric organisms. This is commonly preceded by a significant increase in intestinal colonization with such microbes and with early increases in intestinal permeability, thus suggesting a mechanism of bacterial translocation. Whilst cultures of blood specimens from these patients often remain sterile, it is conceivable that bacteria might translocate in small volumes with detrimental effects but elude detection by standard microbial culture techniques. AIMS: To investigate the incidence and frequency with which bacterial DNA may exist in the systemic circulation of patients with acute pancreatitis and to relate that to disease severity, changes in intestinal permeability, and systemic endotoxin exposure. METHODOLOGY: Blood samples were obtained at admission and on days 3 and 7 from 26 patients with acute pancreatitis (seven with severe cases) and from 10 healthy controls for DNA extraction and standard microbial cultures. Polymerase chain reaction techniques were used to amplify a gene region (16S ribosomal RNA) found in all bacteria. Levels of serum endotoxin and antibodies to endotoxin core (EndoCAb) were measured at admission, and intestinal permeability to the macromolecule polyethylene glycol 3350 was determined within 72 hours of the onset of symptoms. RESULTS: Blood cultures yielded and enterococci for one patient with a severe attack and coagulase-negative staphylococci for another patient with a mild attack. No bacterial DNA was found in any of the samples. Endotoxemia was detected in 20 patients (five with severe cases), and levels of serum IgM EndoCAb were depleted in patients with severe attacks but remained relatively unchanged during mild attacks (p = 0.033). Intestinal permeability was significantly increased in patients with severe attacks of acute pancreatitis but remained unchanged during mild attacks (p < 0.05). CONCLUSIONS: Whilst severe attacks of acute pancreatitis are associated with early derangement in gut barrier function and systemic endotoxin translocation, there is no molecular evidence for associated bacterial "translocation."

Acute Disease↗
PubMed1993

Vasopressin contributes to the cardiovascular response to dynamic exercise.

Vasopressin is a powerful vasoconstrictor that is released into the systemic circulation during exercise. We tested the hypothesis that this peptide contributes to the cardiovascular response during treadmill exercise in the pig. Seventeen miniswine were instrumented with epicardial electrocardiogram leads, left atrial and aortic catheters, and a left ventricular pressure transducer for measurement of heart rate (HR), regional blood flow, arterial blood pressure (MAP), and myocardial contractility [first derivative of left ventricular pressure (dP/dt) at 40 mmHg developed pressure] at rest and during exercise. At a work intensity of 80% of each animal's maximal HR reserve, exercise-induced increases in MAP, HR, dP/dt at 40 mmHg developed pressure, and cardiac output were measured. On a separate day, the workload performed by each animal was replicated in the presence of selective vasopressin V1-receptor inhibition using the specific V1 antagonist, [d(CH2)5Tyr(Me)]arginine vasopressin (10-14 micrograms/kg iv). During exercise, MAP was lower (96 +/- 3 vs. 104 +/- 2 mmHg) and cardiac output was higher (13.5 +/- 0.6 vs. 12.6 +/- 1.0 l/min) in the presence of V1-receptor blockade than during unblocked conditions, respectively. Furthermore, we observed an attenuation of exercise-induced decreases in blood flow to the colon. Increases in vascular resistance in the stomach, small intestine, colon, and pancreas also were diminished by V1-receptor inhibition. However, HR and myocardial contractile responses to exercise were not affected. These results suggest that vasopressin contributes to increases in MAP and to the redistribution of cardiac output during dynamic exercise in the miniswine.

Animals↗
PubMed2002

Enterococcus faecalis produces extracellular superoxide and hydrogen peroxide that damages colonic epithelial cell DNA.

Enterococcus faecalis is a commensal microorganism of the human intestinal tract that produces substantial extracellular superoxide (O(-)(2)), and derivative reactive oxygen species such as H(2)O(2) and hydroxyl radical, through autoxidation of membrane-associated demethylmenaquinone. Because these oxidants may be important as a cause of chromosomal instability (CIN) associated with sporadic adenomatous polyps and colorectal cancer, the ability of E.faecalis to damage eukaryotic cell DNA was examined using the alkaline lysis single cell gel electrophoresis (comet) assay. Both Chinese hamster ovary and HT-29 intestinal epithelial cells showed increased DNA damage after co-incubation with wild-type E. faecalis strain OG1RF, but not a transposon-inactivated mutant with attenuated extracellular O(-)(2) production. E. faecalis-mediated DNA damage was prevented by catalase, but not manganese superoxide dismutase, indicating H(2)O(2) arising from O(-)(2) was the genotoxin. In a rat model of intestinal colonization, OG1RF resulted in significantly higher stool concentrations of H(2)O(2) and 5,5-dimethyl-1-pyrroline N-oxide adducts of hydroxyl and thiyl radicals, as identified by electron spin resonance-spin trapping, compared with rats colonized with a mutant strain having attenuated O(-)(2) production. Using the comet assay, luminal cells from the colon of rats colonized with O(-)(2)-producing E. faecalis showed significantly increased DNA damage compared with control rats colonized with the mutant. These findings suggest a potentially profound role for extracellular free radical production by E. faecalis in promoting CIN associated with sporadic adenomatous polyps and colorectal cancer.

Animals↗
PubMed2003

Giardia duodenalis trophozoites isolated from a parrot (Cacatua galerita) colonize the small intestinal tracts of domestic kittens and lambs.

This study examines the ability of Giardia duodenalis trophozoites, isolated from a wild bird, to colonize the intestinal tracts of companion animals (kittens) and domestic ruminants (lambs). Trophozoites colonized the intestinal tracts of intraduodenally inoculated animals as demonstrated by increasing parasite burdens within the duodenum and jejunum and by fecal passage of cysts within 4 days post-inoculation. The pathogenesis of the trophozoites was further investigated in kittens. In these animals, infection significantly reduced jejunal brush border microvillous length and density, which resulted in a loss of overall epithelial brush border surface area. This injury was associated with the production of diarrhea in four of five infected kittens. These findings indicate that some bird species may carry G. duodenalis that represent a possible health threat to companion animals and livestock. Our results describe the first successful colonization of avian-derived G. duodenalis trophozoites in the small intestines of domestic kittens and lambs.

Animals↗
PubMed1985

Sister chromatid exchange analysis in the colonic and small intestinal epithelium of the mouse.

This report describes a method which produces high quality chromosome preparations from the colon and the small intestine of the mouse. These preparations are suitable for sister chromatid exchange (SCE) analysis because the pretreatment used to dissociate the cells does not prevent sister chromatid differentiation and because very little tissue handling is required at the time of killing, thus allowing sampling from several animals within a short period of time. Since the procedure used to make chromosome preparations from the tissue samples is very simple, no cytogenetic experience is required to make excellent chromosome preparations using this method. To demonstrate the utility of this method, the induction of SCEs by cyclophosphamide was measured in small intestine and colon samples collected from the same animals. The results indicate that this method can be used to determine dose responses in both tissues.

Animals↗
PubMed1989

[Ultrastructural study of the colon after massive intestinal resection in rats].

The modifications suffered by the colon after massive intestinal resection (RIM) have been barely studied, especially from the ultrastructural point of view. On the basis of optical microscope studies we planned this experimental study to evaluate fundamentally the ultrastructural changes in the colonic mucosa and its cellular elements. A total of 115 Wistar rats weighing 350 to 550 grams were used. Twenty animals constituted group 0 (controls), 30 underwent intestinal section (group I) and 65 were submitted to resection of 90% of the intestine (group II). After weighing, the animals were sacrificed by groups on days 15, 30, 45 and 60 of the operation to obtain histologic samples of the ascendant colon for study by transmission (MET) and scanning (MEB) electron microscopy. All the animals resected showed statistically significant weight loss (p less than 0.001), an expression of short intestine syndrome. Groups 0 (controls) and I (intestinal section) did not evidence important ultrastructural changes. In contrast, although in the initial electron microscopic scan the colonic mucosal surface offered a normal aspect, at 45 days it presented irregularities, without the appearance of villi. Days 60 there were deep folds and the mucosal surface had acquired a foliaceous aspect similar to that of the surface of the small intestine of the rat. The abundance of microorganisms adhered to the surface, constituting clumps of bacteria, was striking. Transmission electron microscopy confirmed the greater number and height of the enterocytes, covered by well-developed apical microvilli with dimensions that increased throughout the experiment. The cellular nuclei are voluminous and occasionally have various nucleoli. The cytoplasm showed changes that affected fundamentally the mitochondria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed2006

Effect of vitamin E nutritional supplementation on the pathological changes induced in the ileum of rabbits by experimental infection with enteropathogenic Escherichia coli.

A well-established rabbit model of enteropathogenic E. coli (EPEC) disease was used to examine whether vitamin E (VE) nutritional supplementation had an effect on the pathological changes induced in the bowel by EPEC. Quantitative methods were used to evaluate the influence of VE on bacterial colonization, intestinal mucosal architecture and inflammation, and intestinal epithelial proliferation and apoptosis. VE did not affect EPEC colonization and did not give significant protection against EPEC-induced changes and diarrhoea. Although VE had no effect on the EPEC-related increase of enterocyte apoptosis, it clearly contributed to an acceleration of epithelial cell proliferation in the ileal crypts. This finding may explain why ileal morphometry undertaken in this study showed that VE ameliorated somewhat the effects of EPEC on intestinal mucosal architecture. Quantitative studies on inflammatory cells in the intestinal mucosa revealed that VE nutritional supplementation resulted in an increased neutrophilic and mononuclear inflammatory cell response to EPEC infection, which did not contribute, however, to the clearance of infection.

Animals↗
PubMedDate not supplied

Insulin decreases the secretion of apoB-100 from hepatic HepG2 cells but does not decrease the secretion of apoB-48 from intestinal CaCo-2 cells.

We compared the acute effect of insulin on the human colonic intestinal epithelial cell line CaCo-2 and the transformed human hepatic cell line HepG2. Over 24 h, 100 nM and 10 microM insulin significantly inhibited the secretion of apolipoprotein (apo) B-100 from HepG2 cells to 63 and 49% of control, respectively. Insulin had no effect on the secretion of apoB-48 from CaCo-2 cells. There was no effect of insulin on the cholesterol ester or free cholesterol concentrations in HepG2 or CaCo-2 cells. HepG2 and CaCo-2 cells bound insulin with high affinity, leading to similar stimulation of insulin receptor protein tyrosine kinase activation. Protein kinase C or mitogen-activated protein kinase activity in the presence or absence of insulin was not correlated with apoB-48 production in CaCo-2 cells. Therefore, insulin acutely decreases the secretion of apoB-100 in hepatic HepG2 cells, but does not acutely modulate the production or secretion of apoB-48 from CaCo-2 intestinal cells.

Apolipoprotein B-100↗
PubMed1983

Colonic varices due to intestinal cavernous hemangiomas.

Colonic varices are an unusual cause of rectal bleeding. Occurring most often in the setting of portal hypertension, colonic varices have also been linked to congenital vascular lesions. One such vascular lesion, the cavernous hemangioma, is rarely found in the bowel. We report a patient with cavernous hemangiomas involving skin, lower extremities, and gastrointestinal tract, who presented with chronic rectal bleeding from colonic varices. The progression of his hemangiomatous lesions over an 18-year course is documented. The association of colonic varices and hemangiomas of the bowel is discussed.

Adult↗
PubMed1999

Isolation and chromosomal mapping of a novel human gene showing homology to Na+/PO4 cotransporter.

We isolated a cDNA clone which shows a significant similarity with the renal Na+/phosphate cotransporter (NPT) from a human intestine mucosa cDNA library. The cDNA is 2626 bases long, with one open reading frame encoding a protein of 497 amino acids. The deduced amino acids sequence shows an overall homology of 48% with the human renal NPT1 protein. This gene is expressed in intestine, colon, liver, and pancreas. Thus, this gene may code for intestinal type NPT or closely related proteins. The chromosomal location of the gene was determined on the chromosome 6p21.3-p22 region by polymerase chain reaction-based analysis with both a human/rodent mono-chromosomal hybrid cell panel and a radiation hybrid mapping panel.

Amino Acid Sequence↗