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PubMed1992

Regional differences in gut blood flow and mucosal damage in response to ischemia and reperfusion.

Ischemia and reperfusion of the small intestine and colon in rats were produced by reversible occlusion (for 30 min and 1 or 3 h) of the superior mesenteric artery and the aorta above the inferior mesenteric artery. Despite a greater reduction of mucosal perfusion in the colon than in the small intestine with 30 min of ischemia, the depth of mucosal damage was significantly smaller in the former than in the latter. Thirty minutes of ischemia followed by 1 h of reperfusion induced an increase in polymorphonuclear leukocyte infiltration in both locations. Exacerbation of mucosal injury occurred only in the small intestine, suggesting that reperfusion injury is independent of polymorphonuclear leukocyte infiltration. Reperfusion after 1 or 3 h of ischemia did not exacerbate mucosal damage in either location. Allopurinol significantly diminished the exacerbation of injury after reperfusion in the small intestine. The protective effect of allopurinol, however, was neither associated with an improvement in perfusion nor a reduction in polymorphonuclear leukocyte infiltration. These data indicate that there is a window (30 min) of reperfusion injury in the small intestine, but there is no evidence of reperfusion injury in the colon.

Allopurinol↗
PubMed2003

Delayed viral replication and CD4(+) T cell depletion in the rectosigmoid mucosa of macaques during primary rectal SIV infection.

Rectal infection of macaques by SIV is a model for rectal HIV transmission. We focus here on the digestive tract during days 7-14 of primary rectal infection by SIV in 15 rhesus macaques. Surprisingly, we did not detect productively infected cells in the rectosigmoid colon at early stages of viral dissemination. This strongly suggests that there is no massive viral amplification in the rectosigmoid colon prior to viral dissemination. As dissemination proceeds, productively infected T cells are observed in the rectosigmoid colon and small intestine, with rectosigmoid colon showing the heaviest viral load. Lymphoid follicles are infected prior to lamina propria at both sites. When viral dissemination is widespread, inflammatory infiltrates are visible in the rectosigmoid colon, but not in the small intestine. An important decrease in CD4(+) T cells is then observed in the lamina propria of the rectosigmoid colon only.

Animals↗
PubMed1982

Resistance of mice with limited intestinal flora to enteric colonization by Clostridium botulinum.

Infant botulism is an age-dependent illness that is caused by the toxin produced by Clostridium botulinum infecting the intestinal tract. Because of composition of the intestinal microflora determines the resistance of mice to enteric colonization by C. botulinum, attempts were made to identify the kinds of bacteria that prevent this in vivo growth. Orogastric challenges of 50 spores of C. botulinum type A were given to adult germfree mice, which are highly susceptible, and to gnotobiotic adult mice carrying the eight species comprising the Charles River Altered Schaedler flora or two or three of the limited number of species constituting a different flora (the University of Wisconsin Gnotobiote Laboratory [UW-GL] flora). These floras did not prevent infection due to C. botulinum; however, death rates among the mice with defined floras were significantly lower than those among germfree mice exposed to C. botulinum. Botulinum toxin continued to be produced while animals surviving nearly lethal cases of botulism convalesced slowly but uneventfully. Gnotobiotic mice with the complete UW-GL flora were not infected when challenged with 10(5) spores of C. botulinum.

Animals↗
PubMed1998

Expression of alpha5 (CD49e) and alpha6 (CD49f) integrin subunits on T cells in the circulation and the lamina propria of normal and inflammatory bowel disease colonic mucosa.

Intestinal lamina propria T cells are believed to be derived, via the systemic circulation, from gut-associated lymphoid tissue. After migration into the lamina propria, T cells are capable of luminally directed migration following the loss of surface epithelial cells. For adhesion and migration within the extracellular matrix, T cells are likely to utilize the integrin family of adhesion molecules. The aim of this study was to quantitatively and qualitatively investigate the expression of alpha5 and alpha6 integrin subunits on the surface of human T cells that: (a) migrated out of the lamina propria, (b) remained resident within the matrix and (c) were present in the circulation. In both subpopulations of CD4 and CD8-positive T cells, from both normal and inflamed (inflammatory bowel disease) colonic mucosa, there were significantly fewer alpha5 and alpha6-positive cells than in the peripheral blood. In addition, there were significantly fewer alpha6 integrin molecules on the surface of CD4 and CD8-positive lamina propria T-cell subpopulations, compared with those in the circulation. Our studies suggest that, following migration into the lamina propria, there is down-regulation of alpha5 and alpha6 integrin-subunit expression on the surface of T cells. Molecules other than members of very late activation antigen-5 (VLA-5) (alpha5beta1) and VLA-6 (alpha6beta1) families of adhesion molecules are likely to be important in interactions with extracellular components in the lamina propria of normal and inflamed human colonic mucosa.

Antigens, CD↗
PubMed2001

In vitro effects of wood creosote on enterotoxin-induced secretion measured electrophysiologically in the rat jejunum and colon.

Secretory diarrhea occurs when the balance between intestinal absorption and secretion is disturbed by excessive secretion caused by enterotoxins produced by the pathogen. Wood creosote has long been used as a traditional antidiarrheal remedy. The goal of our study was to extend our knowledge about the antisecretory action of wood creosote against Escherichia coli enterotoxin-induced secretion in the small intestine and colon. Experiments were performed in mucosal sheets of rat jejunum and colon which were stripped of the external muscle layers to eliminate interactions with smooth muscle activity and local blood flow. Mucosal sheets were placed in modified Ussing chambers and hypersecretory conditions were induced by heat-labile (LT) or heat-stable (STa) E. coli enterotoxins added cumulatively (0.01-10 microg/ml) to the mucosal bathing solution. Intestinal secretion was monitored electrophysiologically as transmucosal short circuit current (Isc). LT induced a concentration-dependent increase in Isc in the rat jejunum, with no effect in the colon. In contrast, STa induced a significant increase in colonic Isc, without causing any change in Isc across the jejunum. In separate experiments the effects of increasing concentrations of wood creosote (0.1-50 microg/ml), added to the mucosal or serosal bathing solution, were examined against the secretory responses induced by LT or STa. In the small intestine the antisecretory activity of wood creosote against LT-induced secretion was more potent following serosal application, whereas in the colon wood creosote inhibited STa-induced secretion with equal potency following either serosal or mucosal addition. In summary, our findings demonstrate that wood creosote possesses antidiarrheal activity suppressing E. coli enterotoxin-induced secretion in both the small intestine and colon.

Animals↗
PubMed1994

Octreotide (SMS 201-995) as an antisecretory agent in cholera toxin & bile acid induced intestinal secretion in an in vivo animal study.

The effect of Octreotide (SMS 201-995), synthetic somatostatin analogue on small intestinal and colonic fluid secretion induced respectively by cholera toxin (CT) and deoxycholic acid (DCA) was investigated in rabbits using in vivo isolated loops. After exposure to CT and DCA, marked fluid accumulation was observed in the small intestinal and colonic loops, along with elevation of jejunal and colonic mucosal cyclic AMP concentrations. Octreotide inhibited CT and DCA induced small intestinal and colonic secretion, dose-dependently. This anti-secretory effect was observed after both intramuscular and oral administration of octreotide. In contrast, octreotide did not affect the elevated mucosal cyclic AMP concentrations. These results suggest that octreotide inhibits CT and DCA induced intestinal secretion, and this anti-secretory effect is produced by affecting processes beyond cyclic AMP formation.

Animals↗
PubMed2006

Suppression of gastric acid production by proton pump inhibitor treatment facilitates colonization of the large intestine by vancomycin-resistant Enterococcus spp. and Klebsiella pneumoniae in clindamycin-treated mice.

Proton pump inhibitor treatment of clindamycin-treated mice elevated the gastric pH and facilitated the establishment of colonization of the large intestine by vancomycin-resistant Enterococcus spp. (75 to 80%, versus 20 to 25% for saline-treated controls) and Klebsiella pneumoniae (90%, versus 30% for saline-treated controls). These findings demonstrate a mechanism by which proton pump inhibitor therapy could contribute to the dissemination of nosocomial pathogens.

Animals↗
PubMed2005

Colonization of mucin by human intestinal bacteria and establishment of biofilm communities in a two-stage continuous culture system.

The human large intestine is covered with a protective mucus coating, which is heavily colonized by complex bacterial populations that are distinct from those in the gut lumen. Little is known of the composition and metabolic activities of these biofilms, although they are likely to play an important role in mucus breakdown. The aims of this study were to determine how intestinal bacteria colonize mucus and to study physiologic and enzymatic factors involved in the destruction of this glycoprotein. Colonization of mucin gels by fecal bacteria was studied in vitro, using a two-stage continuous culture system, simulating conditions of nutrient availability and limitation characteristic of the proximal (vessel 1) and distal (vessel 2) colon. The establishment of bacterial communities in mucin gels was investigated by selective culture methods, scanning electron microscopy, and confocal laser scanning microscopy, in association with fluorescently labeled 16S rRNA oligonucleotide probes. Gel samples were also taken for analysis of mucin-degrading enzymes and measurements of residual mucin sugars. Mucin gels were rapidly colonized by heterogeneous bacterial populations, especially members of the Bacteroides fragilis group, enterobacteria, and clostridia. Intestinal bacterial populations growing on mucin surfaces were shown to be phylogenetically and metabolically distinct from their planktonic counterparts.

Bacteria, Anaerobic↗
PubMed2002

Sugar intolerance: origin and mechanisms of symptoms?

The origin and mechanisms of symptoms in sugar intolerance were studied in 8 healthy volunteers. For two test periods, volunteers swallowed a probe with perfused catheters and an infusion catheter which migrated into the colon. A meal containing 40 g lactulose or 40 g sucrose was ingested; the sucrose meal was followed by colonic infusion of 40 g lactulose in order to bypass the small intestine. Recordings of small intestinal and colonic motility were performed. Abdominal pain, bloating, borborygmi, and flatulence were similar during both periods. Both meals increased small intestinal and colonic motility. Only 37% of the symptoms coincided in time with colonic motor events. Symptoms were not related to a specific motor event and were not correlated with breath hydrogen excretion. In conclusion, symptoms of sugar intolerance originate from the colon. They are not related to specific phasic motor events or to breath hydrogen excretion.

Adult↗
PubMed1992

Platelet-activating factor (PAF-acether) formation in neonatal intestinal mucosa and in cultured intestinal epithelial cells.

We report the presence of platelet-activating factor (PAF-acether; 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) in small-intestinal and colonic mucosa of neonatal rats. The PAF-acether content was higher in the colon than in the small intestine, and was lower in the small intestine of 30-day-old animals than in 14-day-old animals. We also report that cultured intestinal epithelial cells (INT 407) produce PAF-acether when stimulated with the calcium ionophore A23187, and that homogenized INT 407 cells can degrade PAF-acether with the formation of lysoPAF-acether. These findings suggest that intestinal epithelial cells are able to produce and metabolize PAF-acether, a potent mediator of inflammation. The authors propose that this might contribute to the pathophysiology of inflammatory bowel disease.

Animals↗
PubMed1990

Distribution and actions of galanin and vasoactive intestinal peptide in the human colon.

Responses to galanin (GAL) and vasoactive intestinal peptide (VIP) and their distribution were investigated in muscularis externa from the human sigmoid colon. Immunohistochemical studies revealed GAL-like immunoreactivity (GAL-IR) and VIP-IR in nerve fibres supplying both muscle layers as well as the myenteric ganglia. Additionally GAL-IR was shown to co-exist with VIP-IR in many nerve fibres innervating human circular and longitudinal (taenial) colonic muscle layers. Circular and longitudinal muscle strips were contracted by GAL and relaxed by VIP. There was a marked difference in sensitivity between muscle layers to both peptides; circular muscle being less sensitive to GAL, longitudinal muscle less sensitive to VIP. When given simultaneously GAL attenuated responses to VIP on longitudinal muscle, thus in the same neurone there are substances having opposing actions on smooth muscle motility.

Colon↗
PubMed2006

Staphylococcus aureus adheres to human intestinal mucus but can be displaced by certain lactic acid bacteria.

There is increasing evidence that Staphylococcus aureus may colonize the intestinal tract, especially among hospitalized patients. As Staph. aureus has been found to be associated with certain gastrointestinal diseases, it has become important to study whether this bacterium can colonize the intestinal tract and if so, whether it is possible to prevent colonization. Adhesion is the first step in colonization; this study shows that Staph. aureus adheres to mucus from resected human intestinal tissue. Certain lactic acid bacteria (LAB), mainly commercial probiotics, were able to reduce adhesion and viability of adherent Staph. aureus. In displacement assays the amount of adherent Staph. aureus in human intestinal mucus was reduced 39-44% by Lactobacillus rhamnosus GG, Lactococcus lactis subsp. lactis and Propionibacterium freudenreichii subsp. shermanii. Moreover, adherent Lactobacillus reuteri, Lc. lactis and P. freudenreichii reduced viability of adherent Staph. aureus by 27-36%, depending on the strain, after 2 h incubation. This was probably due to the production of organic acids and hydrogen peroxide and possibly in the case of L. reuteri to the production of reuterin. This study shows for the first time that Staph. aureus can adhere to human intestinal mucus and adherent bacteria can be displaced and killed by certain LAB strains via in situ production of antimicrobial substances.

Bacterial Adhesion↗
PubMed2001

Colocalization of KCNQ1/KCNE channel subunits in the mouse gastrointestinal tract.

The KCNQI potassium channel alpha-subunit can associate with various KCNE beta-subunits that drastically influence channel gating. Here we show that in the mouse gastrointestinal tract KCNQ1 is prominently expressed in stomach, small intestine and colon, while KCNE3 is expressed in the colon and to a lesser extent in small intestine. Immunostaining revealed that KCNQ1 colocalizes with KCNE3 in the basolateral membranes of crypt cells of the colon and small intestine. Together with the previously shown electrophysiological properties of KCNQ1/KCNE3 channels, this strongly suggests that they form the basolateral potassium conductance that is required for transepithelial cAMP-stimulated chloride secretion. In the stomach, KCNQ1 is expressed together with the H+/K+-ATPase in the luminal membrane of acid-secreting parietal cells of gastric glands. KCNE2, but neither KCNE1 nor KCNE3 was detected in the stomach by Northern analysis. Similar to KCNQ1, KCNE2 was present in gastric glands in only a subset of cells that probably represent parietal cells. The coexpression of KCNQ1 and KCNE2 in HEK293 cells yielded potassium currents that were open at resting voltages, suggesting that these heteromeric channels may underlie the apical potassium conductance in acid-secreting parietal cells that is necessary for the recycling of potassium ions during acid secretion via the H+/K+-ATPase.

Animals↗
PubMed1992

Pharmacokinetics of diltiazem absorption in the rat gastrointestinal tract.

The absorption of diltiazem (CAS 42399-41-7) from the stomach, small intestine, and colon of the rat has been studied, using an in situ cannulation procedure. Diltiazem solutions (1 mg/ml) were prepared in isotonic buffers at pH 3.5 (stomach), 6.2 (small intestine), or 7.5 (colon). 10 ml of drug solution was used in the small intestine, 4 ml was used in the stomach and colon. Aliquot (100 microliters) of the solution was withdrawn at 5-min intervals for a period of 30 min, and assayed by HPLC. A semilog plot of percent remaining vs. time showed that absorption followed apparent first order kinetics with absorption rate constant, ka, equal 0.07 min-1, 0.02 min-1, and 0.01 min-1, in the small intestine, colon, and stomach, respectively.

Absorption↗
PubMed2001

Chemoprevention of intestinal polyposis in the Apcdelta716 mouse by rofecoxib, a specific cyclooxygenase-2 inhibitor.

Mutations in the human adenomatous polyposis (APC) gene are causative for familial adenomatous polyposis (FAP), a rare condition in which numerous colonic polyps arise during puberty and, if left untreated, lead to colon cancer. The APC gene is a tumor suppressor that has been termed the "gatekeeper gene" for colon cancer. In addition to the 100% mutation rate in FAP patients, the APC gene is mutated in >80% of sporadic colon and intestinal cancers. The Apc gene in mice has been mutated either by chemical carcinogenesis, resulting in the Min mouse Apcdelta850, or by heterologous recombination, resulting in the Apcdelta716 or Apedelta1368 mice (M. Oshima et al., Proc. Natl. Acad. Sci. USA, 92: 4482-4486, 1995). Although homozygote Apc-/- mice are embryonically lethal, the heterozygotes are viable but develop numerous intestinal polyps with loss of Apc heterozygosity within the polyps (M. Oshima et al., Proc. Natl. Acad. Sci. USA, 92: 4482-4486, 1995). The proinflammatory, prooncogenic protein cyclooxygenase (COX)-2 has been shown to be markedly induced in the Apcdelta716 polyps at an early stage of polyp development (M. Oshima et al., Cell, 87: 803-809, 1996). We demonstrate here that treatment with the specific COX-2 inhibitor rofecoxib results in a dose-dependent reduction in the number and size of intestinal and colonic polyps in the Apcdelta716 mouse. The plasma concentration of rofecoxib that resulted in a 55% inhibition of polyp number and an 80% inhibition of polyps > 1 mm in size is comparable with the human clinical steady-state concentration of 25 mg rofecoxib (Vioxx) taken once daily (A. Porras et al., Clin. Pharm. Ther., 67: 137, 2000). Polyps from both untreated and rofecoxib- or sulindac-treated Apcdelta716 mice expressed COX-1 and -2, whereas normal epithelium from all mice expressed COX-1 but minimal amounts of COX-2. Polyps from either rofecoxib- or sulindac-treated mice had lower rates of DNA replication, expressed less proangiogenic vascular endothelial-derived growth factor and more membrane-bound beta-catenin, but showed unchanged nuclear localization of this transcription factor. This study showing the inhibition of polyposis in the Apcdelta716 mouse suggests that the specific COX-2 inhibitor rofecoxib (Vioxx) has potential as a chemopreventive agent in human intestinal and colon cancer.

Animals↗
PubMed2005

The Steinernema carpocapsae intestinal vesicle contains a subcellular structure with which Xenorhabdus nematophila associates during colonization initiation.

Steinernema carpocapsae infective juvenile (IJ) nematodes are intestinally colonized by mutualistic Xenorhabdus nematophila bacteria. During IJ development, a small number of ingested X. nematophila cells initiate colonization in an anterior region of the intestine termed the vesicle and subsequently multiply within this host niche. We hypothesize that efficient colonization of a high percentage of S. carpocapsae individuals (typically>85%) is facilitated by bacterial adherence to a site(s) in the nematode intestine. We provide evidence that the adherence site is a structure in the lumen of the IJ vesicle that we have termed the intravesicular structure (IVS). The IVS is an untethered cluster of anucleate spherical bodies that co-localizes with colonizing X. nematophila cells, but does not require X. nematophila for its formation. Colocalization with the IVS is readily apparent in IJs colonized by X. nematophila mutants that initiate intestinal colonization but fail to proliferate normally, suggesting that bacterial-IVS interaction occurs early in the colonization process. Treatment with insect haemolymph induces anal release of X. nematophila from colonized IJs and induces release of the IVS from uncolonized S. carpocapsae IJs. Released IVS were probed with several carbohydrate-specific lectins. One lectin, wheat-germ agglutinin, reacts strongly with a mucus-like substance that is present around individual spheres in the aggregate IVS. Potential roles for the IVS in mediating X. nematophila colonization of the nematode intestine are discussed.

Animals↗
PubMed2000

Application of a biomagnetic measurement system (BMS) to the evaluation of gastrointestinal transit of intestinal pressure-controlled colon delivery capsules (PCDCs) in human subjects.

PURPOSE: For determination of the transit time through various parts of the gastrointestinal (GI) tract, we developed a method that provides the location of disintegration and drug release. This method involves GI magnetomarkergraphy (GIMG) using a 129-channel Shimadzu vector biomagnetic measurement system (BMS). METHODS: To magnetically label the pressure-controlled colon delivery capsule (PCDC) containing 75.0 +/- 0.5 mg of caffeine as a tracer drug, small capsule caps containing 90 mg of ferric oxide powdered magnetite (Fe2O3) were attached to PCDCs. After orally administration to fasted human volunteers, saliva samples were collected hourly and salivary caffeine concentration was measured. At the same time, locations of the magnetic PCDC were detected by BMS just after the PCDCs were magnetized with the coils of a magnetic resonance imaging (MRI) system. The magnetic field distributions were analyzed and the estimated positions were shown on the MRI picture of the same subject's abdominal structure. RESULTS: We magnetized PCDC with permanent magnets or an electromagnet before ingestion and the estimated locations of PCDC in the GI tract exhibited high estimation error. In order to increase the precision of estimated localization of PCDCs, PCDCs were magnetized within the coils of the MRI. As a result, these PCDCs had strong magnetic dipoles that were parallel to the sensor unit of BMS in every measurement, and therefore the spatial resolution of the PCDC's two-dimensional positions in the organs of the GI tract was within a range of several millimeters. CONCLUSIONS: GIMG is a powerful tool for the study of colon delivery efficiencies of PCDCs. The main advantage of GIMG is the capability to obtain even more detailed knowledge of the behavior and fate of solid pharmaceutical formulations during GI passage.

Abdomen↗