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PubMed1988

Colonization resistance of the human intestinal microflora: testing the hypothesis in normal volunteers.

Colonization resistance is the mechanism whereby the intestinal microflora protects itself against incursion by new and often harmful microorganisms. Some authors have claimed that colonization resistance is related to the integrity of the anaerobic flora, but this point has not been established in humans. In previous studies in our laboratory cefoxitin, piperacillin, cefoperazone or aztreonam were administered intravenously to healthy volunteers in order to study changes in the intestinal flora and acquisition of new strains. Seven of 16 antibiotic-treated subjects were colonized with gram-negative bacilli, but no correlation was observed between this colonization and the suppression of either anaerobes or any other component of the fecal flora. Marked strains of Escherichia coli and Pseudomonas aeruginosa were also administered by mouth in order to test acquisition of new bacteria. The fed bacteria were found in the stools of both antibiotic-treated and control subjects; the antibiotics had no apparent influence on the ability of these strains to colonize the intestinal tract. Our work, along with findings of others, supports the concept that colonization resistance occurs in humans and is diminished by antibiotic administration. However, it does not support the hypothesis that colonization resistance is related to the anaerobic microflora.

Anti-Bacterial Agents↗
PubMed1995

Gastrointestinal cancer.

BACKGROUND: There are great differences in incidence and prognosis of cancer among the component sites of the digestive tract. Furthermore, a number of the histologic types of tumors at these sites differ in their incidence and prognosis. METHODS: The SEER data from 1973 to 1987 on frequency, incidence, staging, and survival for the various histologic types of 194,452 cancers of the esophagus, stomach, and intestines were studied. RESULTS: There was an increased incidence of adenocarcinomas of esophagus, gastric cardia, small intestine, and colon; incidence rates for rectal adenocarcinoma and esophageal squamous cell carcinoma remained stable; and rates for gastric adenocarcinoma decreased. Blacks had higher incidence rates than whites for gastric adenocarcinoma; squamous cell carcinoma of the esophagus; carcinoids of the small intestine, colon, and rectum; and gastric sarcomas. Whites, especially males, had higher incidence rates for adenocarcinomas of the esophagus and gastric cardia than did blacks. Blacks had lower rates for rectal adenocarcinomas than did whites, but slightly higher rates than whites for rectal mucinous carcinomas and colonic adenocarcinomas. Data on race, sex, survival, and time trends indicate that mucinous colorectal carcinomas are biologically different from other adenocarcinomas. Males had poorer overall survival than did females for most histologic types of digestive tract tumors. Appendiceal mucinous adenocarcinomas with distant metastases were associated with a high (50%) 5-year survival. The poor prognosis of cases diagnosed as colonic carcinoid raises the possibility that some of these actually may be carcinomas. CONCLUSION: Studies of digestive tract cancer require analysis by histologic type for adequate assessment.

Adolescent↗
PubMed1997

Adherence of Vibrio cholerae to cultured differentiated human intestinal cells: an in vitro colonization model.

Choleragenic vibrios adhered to and multiplied on monolayers of the highly differentiated mucin-secreting cell line HT29-18N2. Their adherence followed first-order kinetics, was dependent on the concentration of vibrios, and was partially inhibited by lipopolysaccharide. Comparison of genetically modified vibrios showed that flagella, an active toxR gene, and the virulence cassette were not essential for initial binding. Inactivation of the hemagglutinin/protease increased binding. This highly differentiated human intestinal cell line provides a versatile new approach for studying major events occurring during intestinal colonization: adherence, multiplication, and detachment.

Bacterial Adhesion↗
PubMed1999

Effect of dietary fiber on intestinal barrier function of 5-Fu stressed rats.

Chemotherapy might damage intestinal barrier function (IBF). The aim of the study was to evaluate the effect of dietary fiber on IBF of 5-fluorouracil (5-Fu) stressed rats. Thirty Wistar rats after gastrostomy were assigned randomly to one of three groups (10 of each group), Chow, enteral nutrition (EN), or EN+Fiber (2 g/100 ml solution). They kept their diets respectively for 8 days. 5-Fu (75 mg/kg body weight) was injected intraperitoneally on day 4. Urinary recovery ratios of lactulose and mannitol (L%/M%) were measured on day 3 and day 7. The mesenteric lymph nodes were harvested for bacterial translocation (BT). On day 8, small intestine and colon were taken for wet weight, mucosal thickness of both small intestine and colon and villus height of small intestine. The BT rates of Chow and EN+Fiber groups (20% for both) were lower than that of EN group (70%) (P<0.05). The L%/M% of both EN+Fiber (from 0.0265+/-0.0073 to 0.0274+/-0.0068) and Chow groups (from 0.0268+/-0.0039 to 0.0281+/-0. 0044) were unchanged after stress (P>0.05 for both), whereas that of EN group significantly increased (from 0.0289+/-0.0070 to 0.0331+/-0. 0084) (P<0.01). Chow group gained body weight (4.9+/-4.3 g). EN+Fiber group lost less body weight (-3.1+/-3.4 g) than EN group (-6.6+/-5.2 g) (P<0.05). The intestinal structure of Chow and EN+Fiber groups was superior to that of EN group. In conclusion, dietary fiber could protect the IBF of 5-Fu stressed rats.

Animals↗
PubMedDate not supplied

The digestive tract after 7 days of restraining conditions in normal and adrenalectomized rats.

Hypokinesia produced specific reactions in tissues related to motion (bones, skeletal muscles and myocardium) and nonspecific in others, as that of the digestive tract after 7 days of hypokinesia. A decreased content of glycoproteins from mucous salivary glands, stomach, small intestine and colon, and an increased intestinal content of leucine-aminopeptidase and acid and alkaline phosphatase were found as a result of histochemical reactions. An important plasmatic corticosterone increase was also found. The same histochemical modifications appeared in adrenalectomized rats in which the plasma corticosterone was substantially diminished. Therefore these glycoproteins and enzymatic secretions are not dependent on the glucocorticoid response.

Adrenalectomy↗
PubMed1984

[Functional colon sonography in neuronal intestinal dysplasia. Report of 3 cases].

For the first time morphology and function of the colon were analysed by sonography in three children with M. Hirschsprung and neuronal-intestinal dysplasia. After one year two children attained almost normalisation of colon-peristalsis in the nonaganglionic segments. A resection of the neuronal-dysplastic segments was not necessary. In one child there was seen no change of the distal colon motility. The limit of resection at operation was determined by sonographic diagnosis following observation of stimulated motility. Sonographic long-time examination in connection with medicamental stimulation of the colon allows determination on timing and kind of therapy in neuronal-intestinal dysplasia.

Age Factors↗
PubMed2006

[Studies on the absorption kinetics of baicalin and baicalein in rats' stomachs and intestines].

OBJECTIVE: To study the absorption kinetics of baicalin and baicalein in rats' stomachs and intestines. METHOD: The drug concentration by in situ perfusion in rats were determined by HPLC. RESULT: The hourly absorption percentages of baicalin in stomach, small intestine and colon were 8.05%, - 0.94% and 2.32%, respectively, and baioalein with 34.53%, 30.61% and 4.89%, respectively. The absorption rate constants of baicalein were 0.090 7, 0.083 7, 0.076 6 and 0.048 3, respectively in duodenum, jejunum, ileum and colon. CONCLUSION: Baicalin is moderately absorbed in stomach and poorly in small intestine and colon; Baicalein is well absorbed in stomach and small intestine but worse in colon, suggesting that the former is more suitable to be administered orally. The extensive absorption segments of bacailein suggests that it can be processed into a sustained-release preparation.

Animals↗
PubMedDate not supplied

The intestinal microflora and the colon cancer connection.

Epidemiologic studies and laboratory research have indicated an association between the metabolic activity of the intestinal microflora and cancer of the large bowel. It has been suggested that activation of procarcinogens could be mediated enzymatically by intestinal bacteria. The levels of incriminated colonic bacterial enzymes are increased by dietary fat and inhibited by certain dietary fibers. Organic extracts of feces contain a mutagenic substance, presumably derived from bacterial metabolism in the large bowel, that is positive in the Ames test. Whether this substance or some other organic chemical is the putative proximate carcinogen remains speculative, but the evidence continues to point to intestinal bacteria as the metabolic intermediary in colon cancer.

Animals↗
PubMed2003

Keratinocyte growth factor and epidermal growth factor can reverse the intestinal atrophy associated with elemental diets in mice.

Elemental diets are associated with intestinal atrophy and reduced intestinal integrity. Growth factors such as keratinocyte growth factor (KGF) and epidermal growth factor (EGF) have considerable potential for the therapeutic reversal of such atrophy and may have greater actions if given in combination. We examined the effects of recombinant human KGF (rHuKGF), EGF and their combination on tissue mass, cell proliferation and crypt fission throughout the intestine of mice fed elemental diets. rHuKGF significantly increased the relative wet weight of the intestine, with EGF having a lesser effect. Cell proliferation of the stomach, small intestine and colon were significantly increased by rHuKGF, but EGF only increased proliferation in the small intestine. Crypt fission in the small intestine and colon was significantly decreased by rHuKGF. An interactive effect of rHuKGF and EGF on the weight of stomach and the proliferation of the fundus and antrum was observed. Moreover, an interactive effect of the agents was also seen on crypt fission in the colon. We concluded that (1) rHuKGF and EGF have significant trophic effects on the stomach, small intestine and colon, (2) these actions vary between different sites in the gastrointestinal tract, and (3) interactive effects occur.

Animals↗
PubMed1985

Colonization of the mouse intestine by an avirulent Salmonella typhimurium strain and its lipopolysaccharide-defective mutants.

For study of the role of lipopolysaccharide (LPS) character in colonization of the mouse large intestine, use was made of S. typhimurium strain SL5316, which is streptomycin resistant and smooth (wild-type LPS) but nonvirulent because it is Aro- (aromatic dependent). Several rough variants of different LPS chemotype derived from strain SL5316 comprised: an rfb deletion transductant making type Ra (complete core) LPS; an rfaJ mutant making incomplete core of type Rb2; and an rfa-990 mutant making LPS core less complete than chemotype Rb2. We tested these strains for colon-colonizing ability by feeding them to male CD-1 mice receiving streptomycin sulfate (5 g/liter) in their drinking water. Each strain, if fed alone, was found in the feces throughout the 15 days of the experiment at about 10(8) CFU/g for the smooth strain or 10(7) CFU/g for each of its rough derivatives. However, when mice were fed equal numbers of two strains (with differentiating antibiotic resistance characters), the strain with the more complete LPS was found in the feces in great excess, 1000- to 100,000-fold, according to the pair. Thus, when strains were placed in direct competition with one another, their relevant colon-colonizing abilities were found to be wild type greater than rfb much greater than rfaJ greater than rfa-990, showing that the ability of a Salmonella strain to colonize the mouse large intestine decreases as its LPS structure becomes more defective.

Animals↗
PubMed1999

Modulation of the permeability of H2 receptor antagonists cimetidine and ranitidine by P-glycoprotein in rat intestine and the human colonic cell line Caco-2.

The influence of secretory transporters on intestinal permeability characteristics of the H2 receptor antagonists ranitidine and cimetidine was studied in Caco-2 monolayers and rat intestinal mucosa mounted in Ussing chambers. Both drugs exhibited vectorial transport across rat ileum with significantly greater (2-4-fold) permeability in the serosal-to-mucosal than the mucosal-to-serosal direction, indicative of net mucosal secretion. Mucosal ranitidine secretion was also observed in rat distal colon, although to a lesser degree. Ileal ranitidine secretion was concentration dependent and significantly reduced by the P-glycoprotein (P-gp) substrates verapamil and cyclosporin. In contrast, probenicid, an inhibitor of the multidrug-related protein, had no effect on ranitidine permeability. The paracellular marker mannitol showed no evidence of asymmetric permeability or sensitivity to P-gp inhibitors. Significant expression of P-gp protein in rat intestinal epithelial cells was confirmed by immunoblotting. Caco-2 monolayers, which overexpress P-gp, also showed asymmetric permeability of ranitidine and cimetidine. In this model, ranitidine permeability in the mucosal-to-serosal direction decreased by approximately 95% as monolayer resistance increased from 150 to 500 Omega/cm2, indicating a primarily paracellular route of transport. However, serosal-to-mucosal permeability was insensitive to resistance changes, consistent with a primarily transcellular route in this direction. These data indicate that ranitidine and cimetidine can act as substrates for intestinal P-gp and suggest that the balance between absorptive and secretory mechanisms as a factor in determining intestinal absorption needs to be a routine consideration even for compounds expected to have a predominantly paracellular route of absorption.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

Release of guanylin immunoreactivity from the isolated vascularly perfused rat colon.

The intestinal peptide guanylin regulates the electrolyte/water transport in the intestinal epithelium. The aim of the present study was to investigate the mechanisms that modulate its secretion in the isolated vascularly perfused rat colon by using a specific guanylin RIA. Intraarterial infusion of bethanechol (10(-4) M) or bombesin (10(-7) M) elicited a significant 6-fold increase in the release of guanylin immunoreactivity (G-IR) in the lumen. Bombesin-stimulated G-IR secretion was strongly reduced by tetrodotoxin, whereas atropine had no effect. VIP (10(-7) M) induced a moderate release of G-IR, whereas substance P, calcitonin gene-related peptide, peptide YY, somatostatin, and neurotensin were without effect. Dimethyl-PGE2 (1.4 x 10(-5) M) or interleukin-1beta (2.5 x 10(-10) M) induced a 3-fold increase in G-IR in the lumen, whereas the degranulator compound bromolasalocid did not stimulate guanylin secretion. Forskolin (10(-5) M) or sodium nitroprusside (10(-4)-10(-3) M) induced a significant release of G-IR. In contrast, PMA (10(-7) M) or ionophore A23187 (10(-6) M) did not modify basal secretion of G-IR. Upon stimulation of guanylin release with bombesin or bethanechol, an increase in G-IR in the portal effluent was also detected. The release of G-IR in the portal effluent was 40-fold lower than that of G-IR into the luminal perfusate. Additionally, analysis with gel chromatography revealed that the immunoreactive material released in the lumen or in the portal effluent coeluted with the 15-amino acid peptide originally isolated from rat intestine. In conclusion, the present data suggest that the enteric nervous system and immune cells may modulate guanylin release from the rat colon. The release of guanylin in the lumen and portal effluent suggests that this peptide may exert both luminal/paracrine and hormonal effects.

Animals↗
PubMed1993

Expression of gap junction connexin 43 and connexin 43 mRNA in different regional tissues of intestine in dog.

To determine the distribution of gap junction protein connexin 43 (Cx43) and the expression of Cx43 mRNA in different regions of canine small intestine and colon, modified Western blot and Northern blot techniques were used with a site-directed antibody raised against a synthetic peptide of Cx43 Anti-Cx43 (252-271) and a probe of 1.3-kb Cx43 cDNA. Equal amounts of plasma membrane enriched fraction (10 micrograms protein) from small intestinal and colonic circular muscle, longitudinal muscle, and colonic submucous plexus border of circular muscle (interstitial cells of Cajal rich layer, ICC) of the dog were resolved by 12% sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred onto nitrocellulose, and blotted by chemiluminescent assay. Different yet characteristic ratios of the immunoreactive gap junction proteins located at 43 and 40 kDa were found in membranes from small intestinal and colonic circular smooth muscle, and ICC. These results suggest that gap junction Cx43 in dog heart, dog small intestinal and colonic circular muscle, and ICC is homologous to rat heart. Furthermore, with the use of Northern blot hybridization with a 1.3-kb Cx43 cDNA, a 3.0-kb message was observed in small intestinal and colonic circular muscles, longitudinal muscles, and ICC. However, the mRNA signal of small intestinal circular muscle was the strongest and that of longitudinal muscle was weakest, especially from colon longitudinal muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed2004

Effects of iron and phytic acid on production of extracellular radicals by Enterococcus faecalis.

Enterococcus faecalis is a human intestinal commensal that produces extracellular superoxide, hydrogen peroxide, and hydroxyl radical while colonizing the intestinal tract. To determine whether dietary factors implicated in colorectal cancer affect oxidant production by E. faecalis, radicals were measured in rats colonized with this microorganism while on diets supplemented with iron or phytic acid. Hydroxyl radical activity was measured by assaying for aromatic hydroxylation products of D-phenylalanine using reverse-phase high-performance liquid chromatography and electrochemical detection. In vitro, as expected, iron enhanced, and phytic acid decreased, hydroxyl radical formation by E. faecalis. For rats colonized with E. faecalis given supplemental dietary iron (740 mg elemental iron as ferric phosphate per kg diet) or phytic acid (1.2% w/w), no differences were found in concentrations of urinary ortho- or meta- isomers of D-phenylalanine compared to rats on a basal diet. Aqueous radicals in colonic contents were further assessed ex vivo by electron spin resonance using 5,5-dimethyl-1-pyrroline-N-oxide as a spin trap. Mixtures of thiyl (sulfur-centered) and oxygen-centered radicals were detected across all diets. In vitro, similar spectra were observed when E. faecalis was incubated with hydrogen sulfide, air-oxidized cysteine, or an alkylsulfide, as typical sulfur-containing compounds that might occur in colonic contents. In conclusion, intestinal colonization with E. faecalis in a rat model generates both thiyl and oxygen-centered radicals in colonic contents. Radical formation, however, was not significantly altered by short-term dietary supplementation with iron or phytic acid.

Animals↗
PubMed1995

Cholera toxin-induced small intestinal secretion has a secretory effect on the colon of the rat.

BACKGROUND/AIMS: Little information is available on the role of colon during small intestinal secretion. The aim of this study was to examine the effects of secretory changes in the small intestine on the colonic transport of electrolytes and water in vivo. METHODS: The jejunum and colon of the rat were perfused in vivo simultaneously but separately, and jejunal secretion was induced by exposing the jejunum to cholera toxin, 8-bromo-cyclic guanosine monophosphate, or hyperosmolarity. RESULTS: Jejunal perfusion with a hyperosmolar mannitol solution (600 mOsm/L) or with 8-bromo-cyclic guanosine monophosphate (0.5 mmol/L) resulted in net secretion of water in the jejunum but did not affect the baseline rate of water transport in the colon. On the contrary, addition of cholera toxin (1 microgram/loop) to the jejunal segment not only induced a significant local secretory change but also resulted in a similar change in the colon, which was not exposed to cholera toxin. The intestine was transected immediately below the jejunum, thus interrupting the anatomical continuity of the enteric nervous system. This procedure eliminated the distant secretory effect of cholera toxin, thus allowing the conclusion that the enteric nervous system is involved in the distant propagation of the local secretion induced by cholera toxin. CONCLUSIONS: Cholera toxin, but not other secretagogues, triggers a secretory response that is not only local but also extends to distal segments via the enteric nervous system.

Animals↗
PubMedDate not supplied

Effect of portal hypertension on bacterial translocation induced by major liver resection in rats.

OBJECTIVE: To evaluate the influence of portal hypertension on bacterial translocation from the gut caused by major hepatic resection. DESIGN: Randomised study. SETTING: University of Lund, Sweden. MATERIAL: 228 adult male Sprague-Dawley rats. INTERVENTIONS: Laparotomy and separation of the liver from its attachments (sham operated group), 70% hepatic resection, 90% hepatic resection, or subtotal ligation of the portal vein. For assessment of the degree of bacterial translocation a further laparotomy was done, 0.2 ml of blood taken from the portal vein and the vena cava, and specimens taken of mesenteric lymph nodes, liver, spleen, lungs, proximal jejunum, distal ileum, and transverse colon. Microcirculation of the intestine was measured by laser Doppler flowmetry with the probe held gently against the bowel wall at six points randomly chosen from the distal small intestine and colon. MAIN OUTCOME MEASURES: Alterations in portal venous pressure, arterial pressure, and bacterial translocation to other organs, particularly mesenteric lymph nodes. RESULTS: Bacterial translocation increased significantly after 90% hepatectomy, and there was an increase in portal pressure together with a decrease in systemic arterial pressure after both 90% hepatectomy and subtotal ligation of the portal vein. Subserosal blood flow to the distal small intestine decreased after 70% resection, 90% resection, and subtotal ligation of the portal vein; subserosal blood flow to the colon decreased only after 90% hepatectomy. CONCLUSION: Increased portal venous pressure after major hepatic resection is not the sole cause of the increase in the incidence of bacterial translocation from the gut in rats.

Animals↗
PubMed2000

Lack of a role of cytotoxic necrotizing factor 1 toxin from Escherichia coli in bacterial pathogenicity and host cytokine response in infected germfree piglets.

Some Escherichia coli strains isolated from intestinal or extraintestinal infections in pigs produce cytotoxic necrotizing factor 1 (CNF1). In order to analyze the role of CNF1 in the pathogenesis of porcine colibacillosis, newborn colostrum-deprived germfree piglets were orally inoculated with a wild-type CNF1-producing strain (M623) or with an isogenic cnf1 mutant (M623DeltaCNF1). The two isogenic strains induced a high mortality with similar lung and serosal inflammatory lesions, indicating that both strains were pathogenic in these piglets. Bacterial counts in various organs of inoculated piglets revealed an intestinal predisposition of M623 and M623DeltaCNF1 strains for the cecum and colon. Extraintestinal organs (lungs, liver, spleen, and kidney) were also colonized by both strains. Similar colonization of intestinal and extraintestinal tissues in animals inoculated with either strain was observed, except in the ileum, where M623 showed a higher colonization than M623DeltaCNF1. Intestinal (ileum and colon), extraintestinal (lung and kidney), and immune (mesenteric lymph nodes and spleen) tissues were sampled at 1 day postinoculation and analyzed for cytokine expression by a reverse transcriptase PCR technique. Inoculation with E. coli M623 induced an enhanced expression of inflammatory cytokines (interleukin-1alpha [IL-1alpha], tumor necrosis factor alpha, and IL-12p40) in the intestinal organs compared to uninoculated piglets or piglets inoculated with nonpathogenic intestinal E. coli 862B, which is also able to colonize the intestinal tract. There was little difference in cytokine transcript levels in the intestinal and extraintestinal organs in piglets inoculated with E. coli strains M623 or M623DeltaCNF1, except in the ileum, where IL-1alpha and IL-8 mRNA levels correlated with bacterial colonization. Expression of regulatory cytokines (gamma interferon and IL-4) was weak in immune tissues from piglets inoculated with M623 or M623DeltaCNF1. Taken together, our data indicate that the CNF1-producing strain, M623, is pathogenic and induces inflammatory cytokine expression in germfree, colostrum-deprived piglets. Nevertheless, in this model, the CNF1 toxin does not appear to be a major factor for pathogenicity or cytokine response, as demonstrated by the use of an isogenic cnf1 mutant.

Animals↗